Toxic Exposures and  Parkinsons  & the Mercury and Toxic Metals Connection

      Bernard Windham (Ed.)- Chemical Engineer/Biostatistician

 

I.                Introduction. 

There has been a huge increase in the incidence of degenerative neurological conditions in virtually all Western countries over the last 2 decades (574,580,598). Neurodegenerative Conditions are increasing due to increased inflammation from vaccinations and excitotoxicity (12b). Much of the damage occurs during brain development which occurs in pregnancy or the first 2 years after birth. Increased glutamate outside neuron cells is a factor in such, triggering excitotoxicity and death of neuron cells. Inflammation from toxic exposures such as toxic metals and pesticides is also a common cause of such damage.

.

Parkinsons   is caused by depletion of dopamine-producing cells in substantia region of brain; (major factors (52,40,33): oxidative stress, inflammation, dysfunctional mitochondria,    susceptibility    factors such as blood allele types, deficiencies,    synergisms    of multiple toxic exposures,    mutation    of neuroprotective genes such as SOD1 and MTHFR, DJ-1); Inflammation caused by vaccines or other sources can trigger microglial priming which causes microglia and macrophages to secrete high levels of inflammatory cytokines which damage neurons(12b). Riboflavin or Thiamin deficiency can be a factor in neurodegeneration & is beneficial(12b): (R5P& B1);  [pesticides and  mercury /metals and toxic bacteria from root canaled teeth or jawbone   cavitations    all cause oxidative stress, inflammation and mitochondrial insufficiency (33,35,56e,108,272,333,573,7) seen in  Parkinsons ,

 

There has been a huge increase in the incidence of degenerative neurological conditions in virtually all Western countries over the last 2 decades (574,303). The increase in  Parkinsons  and other motor neuron disease has been over 50%.   The primary causes appear to be increased exposures to toxic pollutants such as  toxic metals ,  pesticides, herbicides ,  POPs ,  PAHS ,  etc.  resulting in oxidative damage, brain  inflammation   , and mitochondrial damage of free-radicals (27,33,40,52,99,108,272,333,574,580,598).      Most chronic degenerative conditions such as ALS,  ALz , MS, Parkinson’s, CFS, and Cancer have been found to have a combination of immune-system weakening factors often including  (chronic infection from parasites, dental jawbone  infections ( root-canaled teeth or cavitations), other infections); toxic metals; other toxins  (11,33,52). Such conditions usually improve with proper treatment (11,33,52)], however as pointed out by Dr. Yu and other knowledgeable doctors referenced here (11), most doctors and dentists in the U.S. are not properly trained to know what to test for or how to do such tests and have responsibility for some of the huge harm caused these patients. Lyme disease is another factor commonly found to be a factor in chronic degenerative diseases such as MS, Parkinson�s , ALS, etc. (11) L-Carnitine (137a) was protective of damage by low oxygen and impaired blood flow, as well as reducing Autism & ADHD.

 

 

II.        Mercury and toxic metal exposure data

Heavy metal poisoning is extremely common causing oxidative stress, chronic inflammation, and reactive oxidative species which commonly leads to a variety of  autoimmune diseases   and  neurological conditions   including Parkinson�s (8).  Dental amalgam fillings are the largest source of mercury in most people with daily exposures documented to commonly be above government health guidelines (33,49,79,183,199,506,600,217). This is due to continuous vaporization of mercury from amalgam in the mouth, along with    galvanic currents    from mixed metals in the mouth that deposit the mercury in the gums and oral cavity (605,580).  Due to the high daily mercury exposure and excretion into home and business sewers of those with amalgam, dental amalgam is also the largest source of the high levels of mercury found in all    sewers and sewer sludge   , and thus according to government studies a significant source of mercury in rivers, lakes, bays, fish, and crops(603).   People also get significant exposure from vaccinations, fish, and dental office vapor (33,600).

When amalgam was placed into teeth of monkeys and rats, within one- year mercury was found to have accumulated in the brain, trigeminal ganglia, spinal ganglia, kidneys, liver, lungs, hormone glands, and lymph glands (20).  People also commonly get exposures to mercury and other toxic metals such as lead, arsenic, nickel, and aluminum from food, water, and other  sources ( 601,303,592).  All of these are highly neurotoxic and are documented to cause neurological damage which can result in chronic neurological conditions over time, as well as ADHD, mood, and behavioral disorders (580,598,601,602,303).  A study found that those with occupational exposure to lead, arsenic, or copper have more than double the incidence of  Parkinsons  than normal (560). 

 

III.                Toxicity Effects of Mercury and Toxic Metals and other Toxics

  Mercury is one of the most toxic substances in existence and is known to bioaccumulate in the body of people and animals that have chronic exposure (600).  Mercury exposure is cumulative and comes primarily from 4 main sources: silver(mercury) dental fillings, food (mainly fish), vaccinations, and occupational exposure. Whereas mercury exposure from fish is primarily methyl mercury and mercury from vaccinations is thimerosal (ethyl mercury), mercury from occupational exposure and dental fillings is primarily from elemental mercury vapor. Developmental and neurological conditions occur at lower levels of exposure from mercury vapor than from inorganic mercury or methyl mercury (606).  Mercury in amalgam fillings,  because of its high vapor pressure and galvanic action with other metals in the mouth, has been found to be continuously vaporized and  released into the body, and has been found to be  the directly correlated to the  number of amalgam surfaces and the largest source of mercury in the majority of people (49,183,199,209,79,99,600), typically between 60 and 90% of the total.    The level of daily exposure of those with several amalgam fillings commonly exceeds the U.S. EPA health guideline for daily mercury exposure of 0.1 ug/kg body weight/day, and the oral mercury level commonly exceeds the mercury MRL of the U.S. ATSDR of 0.2 ug/ cubic meter of air (217,600).   When amalgam fillings are replaced, levels of mercury in the blood, urine, saliva, and feces typically rise temporarily but decline between 60 to 90% within 6 to 9 months (79,600.).

The main factors determining whether chronic conditions are induced by metals appear to be exposure and genetic    susceptibility   , which determines individuals immune sensitivity and ability to detoxify metals(32,405).  Very low levels of exposure have been found to seriously affect relatively large groups of individuals who are immune sensitive to toxic  metals, or  have an inability to detoxify metals   due to such as deficient  sulfoxidation  or metallothionein function or other inhibited enzymatic processes related to detoxification or excretion of metals.

IV. Mechanisms by which mercury causes neurological conditions found in  Parkinsons  and neurodegenerative diseases.  

Programmed cell death(apoptosis) is documented to be a major factor in degenerative neurological conditions like ALS,  Alzheimers  , MS,  Parkinsons  , etc.  Some of the factors documented to be involved in apoptosis of neurons and immune cells include inducement of the inflammatory cytokine Tumor Necrosis Factor-alpha(  TNFa  ) (126), reactive oxygen species and oxidative stress(13,43a,56a,296b,495), reduced glutathione levels(56,126a,111a), liver enzyme effects and inhibition of protein kinase C and cytochrome P450(43,84,260), nitric oxide and  peroxynitrite  toxicity (43a,521,524), excitotoxicity and lipid peroxidation(496), excess free cysteine levels (56d,111a,30,330),excess glutamate toxicity(13b, 416), excess dopamine toxicity (56d,13a), beta-amyloid generation(462), increased calcium influx toxicity (296b,333,416,432,462c,507) and DNA fragmentation (296,42,114,142) and mitochondrial membrane dysfunction (56de, 416).   Individuals with low glutathione levels were linked with decreased physical performance, increased oxidative stress and impaired redox metabolism of erythrocytes. Excitotoxicity has been shown to be a significant factor in Parkinson�s & other degenerative neurological conditions. (11ab) NAC supplementation restored both performance and redox homeostasis (6 )   .

 Mitochondrial DNA mutations or dysfunction is fairly common , found in at least 1 in every 200 people (275), and toxicity effects affect this population more than those with less susceptibility to mitochondrial dysfunction. This has been found to be a factor in conditions like  Parkinsons  .   The mechanisms by which mercury  causes( often  synergistically    along with other toxic exposures) all of these conditions and neuronal apoptosis will be documented.  

TNFa   (   tumor necrosis factor-alpha) is a cytokine that controls a wide range of immune cell response in mammals, including cell death(apoptosis) in neuronal and immune cells.   This process is involved in inflammatory and degenerative neurological conditions like ALS, MS,  Parkinsons  , rheumatoid arthritis, etc.  Cell signaling mechanisms like sphingolipids are part of the control  mechansim  for the  TNFa  apoptosis mechanism(126a).   Gluthathione  is an amino acid that is  a   normal  cellular mechanism for controlling apoptosis.  When glutathione is depleted in the brain, reactive oxidative species increased, and CNS and cell signaling  mechinsisms  are disrupted by toxic exposures such as mercury, neuronal cell apoptosis results and neurological damage.    Mercury has been shown to induce  TNFa  and deplete glutathione, causing  inflamatory  effects and cellular apoptosis in neuronal and immune cells  (126b,126c). 

          Mercurys  biochemical damage at the cellular level include DNA damage, inhibition of DNA and RNA synthesis (42,114,142,197,296,392);  alteration of protein structure (30,111,114,194,252,442);  alteration of the transport of calcium(333,43b,254,263,416,462,507);  inhibitation  of glucose transport(338,254), and of enzyme function, protein transport, and other essential nutrient transport (96,198,254,263,264,33,330,331,338,339,347, 441,442);  induction of free radical formation(13a,43b,54,405,424), depletion of cellular  gluthathione  (necessary for detoxification processes) (111,126,424,32), inhibition of glutathione peroxidase enzyme(13a,442), inhibits glutamate uptake(119,416), induces  peroxynitrite  and lipid peroxidation damage(521b,119b), causes abnormal migration of neurons in the cerebral cortex(149),   immune system damage (34,111,194, 226,252,272,316,325,355); and inducement of inflammatory cytokines (126,181).

 

Oxidative stress and reactive oxygen species (ROS) have been implicated as major factors in neurological disorders including stroke,  Parkinson�s  Disease (PD),  Alzheimer� s  , ALS,  etc.( 13,424,442.303). Mercury induced lipid peroxidation has been found to be a major factor in mercury�s neurotoxicity, along with leading to decreased levels of glutathione peroxidation and superoxide  dismustase  (SOD) (13,441,443).  Only a few micrograms of mercury severely disturb cellular function and inhibit nerve growth (147,149,226,255, 305,442).   Exposure to mercury results in metalloprotein compounds that have genetic effects, having both structural and catalytic effects on gene expression (114,241,296,442). Mercury inhibits sulfur ligands in MT and in the case of intestinal cell membranes inactivates MT that normally bind cuprous ions (477,114), thus allowing buildup of copper to toxic levels in many and malfunction of the Zn/Cu SOD function (495,13a, 443).      Mercury also causes displacement of zinc in MT and SOD, which has been shown to be a factor in neurotoxicity and neuronal diseases (405,495,517). Some of the processes affected by such metalloprotein control of genes include cellular respiration, metabolism, enzymatic processes, metal-specific homeostasis, and adrenal stress response systems.  Significant physiological changes occur when metal ion concentrations exceed threshold levels.  Such metalloprotein formation also appears to have a relation to autoimmune reactions in significant numbers of people (114,60,313,342,368,369,405, 442). Increased formation of reactive oxygen species (ROS) has also been found to increase formation of advanced glycation end products (AGEs) that have been found to cause activation of glial cells to produce superoxide and nitric oxide, they can be considered part of a vicious cycle, which finally leads to neuronal cell death in the substantia nigra in  PD( 424). 

         Mercury exposure causes high levels of oxidative stress/reactive oxygen species (ROS) (13), which has been found to be a major factor in apoptosis and neurological disease (56,250,441,442,443,13) including dopamine or glutamate related apoptosis(288c).  Mercury and quinones form conjugates with thiol compounds such as glutathione and cysteine and cause depletion of glutathione, which is necessary to mitigate reactive damage.  Such  congugates  are found to be highest in the brain substantia nigra with similar  congugates  formed with L-Dopa and dopamine in  Parkinsons   disease (56).  Mercury depletion of GSH and damage to cellular  mitochrondria  and the increased lipid peroxidation in protein and DNA oxidation in the brain appear to be a major factor in  Parkinsons  disease (30,56,442). Exposure to mercury vapor and methyl mercury is well documented to commonly cause conditions involving tremor and/or ataxia, with populations exposed to mercury experiencing tremor on average proportional to exposure level (250,565,98). Mercury causes the kinds of tremor seen in PD and MS.   �Based on the similar intention tremor in multiple sclerosis and mercury intoxication, human pathology studies in multiple sclerosis, and animal experiments with mercury, it appears that axonal demyelination underlay this form of tremor in both conditions, the former restricted to the CNS and the second to peripheral nerves (565). Occupational and chronic exposure to solvents and metals is considered a possible risk factor for  Parkinson� s   disease  and essential tremor. While manufacturing dental prostheses, dental technicians are exposed to numerous chemicals that contain toxins known to affect the central nervous system, such as n-hexane and mercury (9). we invited 27 dental technicians in an office to undergo a neurological examination. Of the 14 subjects who underwent the neurological examination, four had postural tremor and one had a diagnosis of Parkinson's disease.

One study found higher than average levels of mercury in the blood, urine, and hair of  Parkinsonsdisease  patients (363).  Another study (169) found blood and urine mercury levels to be very strongly related to  Parkinsons  with odds ratios of approx. 20 at high levels of Hg exposure.  Other studies (145) that reviewed occupational exposure data found that occupational exposure to manganese and copper have high odds rations for relation to PD, as well as multiple exposures to these and lead, but one study noted that this effect was only seen for exposure of over 20 years. Occupational exposure to mercury has been found to cause   Parkinsons  (98). One study found the EDTA chelation was effective in reducing some of the effects (145b).

Glutamate is the most abundant amino acid in the body and in the CNS acts as  excitory   neurotransmitter (346,386), which also causes inflow of calcium.   Astrocytes, a type of cell in the brain and CNS with the task of keeping clean the area around nerve cells, have a function of neutralizing excess glutamate by transforming it to glutamic acid.  If astrocytes are not able to rapidly neutralize excess glutamate, then a buildup of glutamate and calcium occurs, causing swelling and neurotoxic effects (119,333). Food flavorings such as MSG are also excitotoxic (11).  Mercury and other toxic metals inhibit astrocyte function in the brain and CNS (119), causing increased glutamate and calcium related neurotoxicity (119,333,226) which are responsible for much of the fibromyalgia symptoms.  This is also a factor in conditions such as CFS,  Parkinsons  , and ALS (346,416,11). 

Parkinson's disease involves the aggregation of alpha-synuclein to form fibrils, which are the major constituent of intracellular protein inclusions (Lewy bodies and Lewy neurites) in dopaminergic neurons of the substantia nigra (564). Occupational exposure to specific metals, especially manganese, copper, lead, iron, mercury, aluminum, appears to be a risk factor for Parkinson's disease based on epidemiological studies (98,145,518,564,580). Elevated levels of several of these metals have also been reported in the substantia nigra of Parkinson's disease subjects (564,580,518). 

Exposure to aluminum hydroxide in vaccines also appears to sometimes cause symptoms similar to   Parkinsons  or other neurological conditions (592).

 

Na( + ),K (+)-ATPase is a transmembrane protein that transports sodium and potassium ions across cell membranes during an activity cycle that uses the energy released by ATP hydrolysis.  Mercury is documented to inhibit  Na( + ),K (+)-ATPase function at very low levels of exposure(288ab). Studies have found that in  Parkinsonscases there was an elevation in plasma serum digoxin and a reduction in serum magnesium, RBC membrane  Na (+)-K+ ATPase activity  (263).   The activity of all serum free-radical scavenging enzymes, concentration of glutathione, alpha tocopherol, iron binding capacity, and ceruloplasmin decreased significantly in PD, while the concentration of serum lipid peroxidation products and nitric oxide increased . .  The inhibition of Na+-K+ ATPase can contribute to increase in intracellular calcium and decrease in magnesium, which can result in 1) defective neurotransmitter transport mechanism, 2) neuronal degeneration and apoptosis, 3) mitochondrial dysfunction, 4) defective  golgi  body function and protein processing dysfunction.  It is documented in this paper that mercury is a cause of most of these conditions seen in  Parkinsons  (13a,111,288,442,521b,43,  56,etc.  )

 Many studies of patients with major neurological or degenerative diseases have found evidence amalgam fillings may play a major role in development  of   conditions  such as such as  Alzheimers  (66,67,158,166,204, 207,221,242,244,257,295,300), ALS(92,97,325,442), MS(102,163,170,184,212,213,285,291,302,324,326),   Parkinsons(98,145,169,248,250,256,258, 363,405,56,84), etc.  Mercury exposure causes high levels of oxidative stress/reactive oxygen  species ( ROS)(13), which has been found to be a major factor in neurological disease(56).  Mercury and quinones form conjugates with thiol compounds such as glutathione and cysteine and cause depletion of glutathione, which is necessary to mitigate reactive damage.  Such  congugates  are found to be highest in the brain substantia nigra with similar  congugatesformed with L-Dopa and dopamine in  Parkinsons     disease( 56,442 ).  Mercury depletion of GSH and damage to cellular  mitochrondria  and the increased lipid  perxodation  in protein and DNA oxidation in the brain appear to be a major factor in  Parkinsons   disease (30,56,442). 

 

       An EKM system for evaluating nerve and muscle function ability using a set of 5  measures  (  precision, imprecision, tremor,  Fitts'  constant, and irregularity) and tested on a group of Cree Indians with mercury exposure from fish eating(565).   Ninety-six participants, including 30 controls subjects, 36 Cree subjects exposed to mercury, 21 subjects with Parkinson disease, 6 with presumed cerebellar deficit, and 3 with essential tremor, participated in the study.  An ANOVA on the three largest groups generated significant results for tremor,  Fitts'constant , and irregularity between the Cree and the control subjects and on  Fitts'  constant and irregularity between the subjects with Parkinson's disease and the control subjects.  Three subgroups of the same mean age composed of six subjects each were selected. One was composed of Cree subjects with the highest level of mercury exposure, another with Cree subjects having a low level of mercury exposure, and a third with control subjects.   An ANOVA on these three groups revealed a significant difference between both groups of Cree subjects and the control group for  Fitts'  constant and irregularity. These preliminary results suggest that the EKM system is able to discriminate the performance of different groups of subjects and found significant evidence that mercury exposure is related to nerve and muscle function conditions such as tremor and   Parkinsons  ( 565). 

 

 Though mercury vapor and organic mercury readily cross the blood-brain barrier, mercury has been found to be taken up into neurons of the brain and CNS without having to cross the blood-brain barrier, since mercury has been found to be taken up and transported along nerve axons as well through calcium and sodium channels and along the olfactory  path( 329, 288,333,34).  Exposure to inorganic mercury has significant effects on blood parameters and liver function. Studies have found that in a dose dependent manner, mercury exposure causes reductions in oxygen consumption and availability, perfusion flow, biliary secretion, hepatic ATP  concentration,  and  cytochrome P450 liver content(260), while increasing blood hemolysis products and tissue calcium content and inducing heme oxygenase, porphyria, and platelet aggregation through interfering with the sodium pump.  

     Studies have found mercury and lead cause autoantibodies to neuronal proteins, neurofilaments, and myelin basic  protein( MBP ) (39b,269ag,405,478,515,516).  Mercury and cadmium also have been found to interfere with zinc binding to  MBP ( 517b) which affects MS symptoms since zinc stabilizes the association of MBP with brain myelin(517a).  MS has also been found to commonly be related to inflammatory activity in the CNS such as that caused by the reactive oxygen species and cytokine generation caused by mercury and other toxic metals (405,478,515,126,303,516,35c). Antioxidants like lipoic acid which counteract such free radical activity have been found to alleviate symptoms and decrease demyelination (494,572).   A group of metal exposed MS patients with amalgam fillings were found to have lower levels of red blood cells, hemoglobin,  hemocrit  , thyroxine, T-cells, and CD8+ suppresser immune cells than a group of MS patients with amalgam replaced, and more exacerbations of MS than those without(102a).  Immune and autoimmune mechanisms are thus seen to be  a   major  factor in neurotoxicity of metals.    Mercury penetrates and damages the blood brain barrier allowing penetration of the barrier by other substances that are neurotoxic (20,38,85,105,301,311/262).  Such damage to the blood brain  barrier�s  function has been found to be a major factor in chronic neurological diseases such as MS and studies have found mercury related mental effects to be indistinguishable from those of MS patients (207,212,222,244,271,286,289,291,302,324,326,183,184).  MS patients have been found to have much higher levels of mercury in cerebrospinal fluid compared to controls (163,35,139). Large German studies including studies at German universities have found that MS patients usually have high levels of mercury body burden, with one study finding 300% higher than controls (271).  Most recovered after mercury  detox ( 369,32), with some requiring additional treatment for viruses and intestinal dysbiosis.  Similarly     thousands of MS patients    have been documented to have recovered or significantly improved after amalgam replacement (35,212,228,291,302,600, etc.)

 

       Mercury has been found to accumulate preferentially in the primary motor function related areas such as the brain stem, cerebellum, rhombencephalon, dorsal root ganglia, and anterior horn motor neurons, which enervate the skeletal muscles (20,291,327,329,442,48). There is considerable indication this may be a factor in development of ALS and other neurodegenerative conditions (48,325,405,442). Treatment using IV glutathione, vitamin C, and minerals has been found to be very effective in the stabilizing and amelioration of some of these chronic neurological conditions by neurologists such as Perlmutter in Florida (469). 

Damage to the locus  ceruleus  , with a subsequent decrease of CNS noradrenaline, occurs in a wide range of neurodegenerative, demyelinating and psychiatric disorders (10). Recently, inorganic mercury was found to enter human locus  ceruleus  neurons selectively. Some Toxicants enter locus  ceruleus  neurons selectively, aided by the extensive exposure these neurons have to CNS capillaries, as well as by stressors that upregulate locus  ceruleus  activity. The resulting noradrenaline dysfunction could affect a wide range of CNS cells and could trigger a number of neurodegenerative conditions (Alzheimer's, Parkinson's and motor neuron disease), demyelinating (multiple sclerosis), and psychiatric (major depression and bipolar disorder).

        Low levels of toxic metals have been found to inhibit  dihydroteridine  reductase, which affects the neural system function by inhibiting brain transmitters through its effect on phenylalanine, tyrosine and tryptophan transport into neurons (122,257,258,289,372). This was found to cause severe impaired amine synthesis and hypokinesis. Tetrahydro-biopterin, which is essential in production  of   nerurotransmitters  , is significantly decreased in patients with  Alzheimers  ,  Parkinsons  , and MS. Such patients have abnormal inhibition of neurotransmitter production ( 432 )( supplements which inhibit breach of the blood brain barrier such as bioflavonoids have been found to slow such neurological damage).

          Clinical tests of patients with MND, ALS,  Parkinson� s  ,   Alzheimers  , Lupus (SLE), and rheumatoid arthritis have found that the patients generally have elevated plasma cysteine to sulphate ratios, with the average being 500% higher than controls (330,331,56), and in general being poor  sulphur  oxidizers.    Mercury has been shown to diminish and block  sulphur  oxidation and thus reducing glutathione levels which is the part of this process involved in detoxifying and excretion of toxics like mercury (30,442,32). Glutathione is produced through the  sulphuroxidation side of this process. Low levels of available glutathione have been shown to increase mercury retention and increase toxic effects (111), while high levels of free cysteine have been demonstrated to make toxicity due to inorganic mercury more severe (333,194,56).  Mercury has also been found to play a part in neuronal problems through blockage of the P-450 enzymatic process (84).  Other toxic metals and toxics such as pesticides have also been found to cause the types of damage seen in  Parkinsons  and to exposure to have positive correlation to  Parkinsons  (27,400,98,145).  Another exposure that affects some appears to be hexane (505).   There are   synergistic effects    of various toxics that result in conditions like  Parkinsons  (524b,13c).  Determination of your factors by history assessment and tests is a first step in improving the condition. 


Susceptibility is a major factor in neurological and immune system damage from toxics such as mercury (490,33,  www.myflcv.com/suscept.html   ). Superoxide  dysmustase  (SOD) is a major and vital factor in the methylation process that produces glutathione (GSH), the body systems master protector from toxic damage, SOD1 gene is neuroprotective but the mutated form SOD1-G93A is not protective, resulting in lower glutathione levels (490). Because of this, the mutated gene form is associated with familial AD as well as being a factor in AD and other conditions by reduced glutathione availability. Mercury vapor and methyl mercury cause significant damage to SOD1-G93 cells but not SOD1 cells(490c). Resveratrol was found to counteract this damage/effect. Apolipoprotein APOE4, one of the 3 blood allele types of APOE, has been found to result in inability to detoxify cells and the body and is a major susceptibility factor in AD and other neurological conditions (113). APOE2 allele people have less susceptibility to toxic effects. APOE3 allele people have more susceptibility than for type 2. People are exposed to a large number of toxic metals and toxins.   Interactions among components of a mixture may change  toxicokinetics  and  toxicodynamics  , resulting in additive or synergistic neurological effects (18).Mercury, aluminum, cadmium, arsenic, some pesticides, and metal based nanoparticles cause types of damage seen in AD and PD(18b), while lead, manganese, solvents, some pesticides cause types of damage seen in PD. Mercury, lead, arsenic, and cadmium induce Fe, Cu, and Zn  dyshomeiostatis  which can result in AD, PD, etc.(18c)

Glutathione is produced by methylation that is responsible for brain neurotransmitter production, immune function, and detoxification. DNA methylation and other epigenetic factors are important in the pathogenesis of late-onset Alzheimer's disease (LOAD). Methylenetetrahydrofolate reductase  (  MTHFR  ) gene mutations occur in most elderly patients with memory loss (36). MTHFR is critical for production of S-adenosyl-l-methionine (SAMe), the principal methyl donor. A common mutation (1364T/T) of the cystathionine-γ-lyase (  CTH  ) gene affects the enzyme that converts cystathionine to cysteine in the  transsulfuration  pathway causing plasma elevation of total homocysteine (  tHcy  ) or  hyperhomocysteinemia  -a strong and independent risk factor for cognitive loss, AD, and other neurological conditions. Other causes of  hyperhomocysteinemia  include aging, nutritional factors, and deficiencies of B vitamins. 

A study (477c) found    that PARK2 mutant  neuroprogenitors  showed increased cytotoxicity with copper (Cu) and cadmium (Cd) exposure. PARK2 mutant  neuroprogenitors  also showed a substantial increase in mitochondrial fragmentation, initial ROS generation, and loss of mitochondrial membrane potential following Cu exposure.

        One genetic difference found in animals and humans is cellular retention differences for metals related to the ability to excrete mercury (426).  For example, it has been found that individuals with genetic blood factor type APOE-4 do not excrete mercury readily and bioaccumulate mercury, resulting in susceptibility to chronic autoimmune conditions such as  Alzheimers  ,   Parkinsons  , etc. as early as age 40, whereas those with type APOE-2 readily excrete mercury and are less susceptible.  Those with type APOE-3 are intermediate to the other 2 types (437,35).  

  The Huggins Clinic Method & IAOMT Safe Replacement Protocol (35,3) using total dental revision (TDR) has been used to successfully treat thousands of patients with chronic autoimmune conditions like MS,  Parkinsons  , Lupus, ALS, AD, diabetes, etc., with an initial population of over 1000(approx. 85%) who experienced significant improvement in MS.   Jaw bone cavitations were found to be common significant factors in some of these conditions such as   Parkinsons  (35,33,580). 

 Huggins Total Dental Revision Protocol (35) or IAOMT Safe Removal Protocol (3) 

(a) history questionnaire and panel of tests.

(b) replace amalgam fillings starting with filling with highest negative current or highest negative quadrant, with supportive vitamin/mineral supplements.

extract all root canaled teeth using proper finish protocol.

(d) test and treat cavitations and amalgam tattoos where relevant

(e) supportive supplementation, periodic monitoring tests, evaluate need for further treatment (not usually needed).

 (f) avoid acute exposures/challenges to the immune system on a weekly 7/14/21 day pattern.

 

 Tests suggested by Huggins/Levy (35) for evaluation and treatment of mercury toxicity:

(a) hair element test (386) (low hair mercury level does not indicate low body  level)(  more than 3 essential minerals  out of normal range indicates likely metals toxicity)

(b) CBC blood test with differential and platelet count

 blood serum profile

(d) urinary mercury (for person with average exposure with amalgam fillings, average mercury level is 3 to 4 ppm; lower test level than this likely means person is poor  excretor  and accumulating mercury, often mercury toxic (35)  

(e) fractionated porphyrin urine test (note test results sensitive to light, temperature, shaking)

(f) individual tooth electric currents (replace high negative current teeth first)

(g) patient questionnaire on exposure and symptom history

(h) specific gravity of urine (test for pituitary function,  s.g  >1.022 normal;  s.g  . < 1.008 consistent with depression and suicidal tendencies (35)}

 

     Note: during initial exposure to mercury the body marshals immune system and other measures to try to deal  with  the challenge, so many test indicators will be high; after prolonged exposure the body and immune system inevitably lose the battle and measures to combat the challenge decrease- so some test indicator scores decline. Chronic conditions are common during this phase. Also high mercury exposures with low hair mercury or  urine  mercury   level usually indicates body is retaining mercury and likely toxicity problem(35).  In such cases where (calcium> 1100 or < 300 ppm) and low test mercury, manganese, zinc, potassium; mercury toxicity likely and  hard  to  treat since retaining mercury.

      Test results indicating mercury/ metals  toxicity ( 35): 

(a) white blood cell count >7500    or < 4500

(b)   hemocrit   > 50%   or < 40%

   lymphocyte count > 2800 or < 1800

(d) blood protein level > 7.5 gm/100 ml

(e) triglycerides > 150 mg %ml

(f) BUN > 18 or < 12

(g) hair mercury > 1.5 ppm    or <   .4 ppm

(h) oxyhemoglobin level < 55% saturated

(I)  carboxyhemoglubin  > 2.5% saturated

(j) T lymphocyte count < 2000

(k) DNA damage/cancer

(l) TSH > 1 ug

(m) hair aluminum > 10 ppm

(n) hair nickel > 1.5 ppm

(o) hair manganese > 0.3 ppm  

(p) immune reactive to mercury, nickel, aluminum, etc.

(q) high hemoglobin and  hemocrit  and high alkaline phosphatase (  alk   phos  ) and lactic  dehydrogenese  (LDA) during initial phases of exposure; with low/marginal hemoglobin and  hemocrit  plus low oxyhemoglobin during long- term chronic fatigue phase.

      note: after treatment of many cases of chronic autoimmune conditions such as MS, ALS,  Parkinsons  , Alzheimers  , CFS, Lupus, Rheumatoid Arthritis, etc., it has been observed that often mercury along with root canal toxicity or cavitation toxicity are major factors in these conditions, and most with these conditions improve after TDR if protocol is followed carefully(35).

 

  There are extensive documented cases (many thousands) where removal of amalgam fillings led to cure of serious health problems such as MS(94,95,102,170,212,213,222,271,291,302, 34 ,35,229,405), ALS(229,325,405,535,35),  Parkinsons  / muscle tremor (222,228,248,229,233c,271,212,322,469,557,94,98,35), Alzheimers (204,35), muscular/joint pain/ fibromyalgia (222,293,317,322,369,35,94),  anxiety & mental confusion (94,212,222,229,233,271,317,303,320,322,57,35), Chronic Fatigue Syndrome (212,293,229,222,232,233,271,313,317,303,320,368,369, 376,595,35), memory disorders(94,222,303,595,35)

Medical studies and doctors treating  fibromylagia  have found that supplements which cause a decrease in glutamate or protect against its effects have a positive effect on fibromyalgia.  Some that have been found to be effective in treating metals related autoimmune conditions such as  Parkinsons  include Vit B6, CoenzymeQ10, methyl  cobalamine  (B12), L-carnitine, choline, ginseng, Ginkgo biloba, vitamins C and E, nicotine,  octacosanol  ,   phosphatifylserine,and   omega 3 fatty acids(fish and flaxseed oil),  tumeric  , lipoic acid, proteolytic enzymes ,and Hydergine(417,444,580).   Reduced  glutathione ( GSH) and N-acetyl cysteine(NAC) have been found to be protective against cellular apoptosis seen in  Parkinsons  and other neurodegenerative conditions( 56ab,462c, 149b).  High levels of Vitamins C and E along with zinc (517) have also been found protective against oxidative stress and some effects of mercury toxicity including for  Parkinsons  (41,63,462c,580,56a). CoQ10 at 600 mg per day was found effective at reducing  Parkinsons  effects (580). IGF-1 treatments have also been found to alleviate some of the symptoms of  ALS ( 424). There is also evidence that melatonin and curcumin may have beneficial effects on reducing metal  toxicity ( 591,497,580).  Turmeric/curcumin has been found to reduce some of the toxic and inflammatory effects of toxic metals. Lithium supplements (lithium carbonate and lithium  oratate  ) have been found to be effective in protecting neurons and brain function from oxidative and excitotoxic effects.  A recent study demonstrated that combined treatment with lithium and valproic acid elicits synergistic neuroprotective effects against glutamate excitotoxicity in cultured brain neurons (590).  

Doctors affiliated with Life Enhancement Foundation have developed a diet and supplementation protocol to reduce  Parkinsons  effects and delay the start time of daily levodopa therapy (page 1139) (580).  Dietary considerations include avoidance of alcohol, sugar, red meats, cow�s milk products, gluten, fried foods, aspartame, MSG, pesticides.   

 

Some clinics have found root canals, cavitations , and amalgam tattoos to also be a factor in such autoimmune conditions and that treatment of them improves prognosis in recovery from these   conditions  (35,437,580). 

Vitamin C homeostasis is essential to Brain Health

Vit C is a nutrient of great importance for proper functioning of nervous system and its main role in the brain is its participation

in the antioxidant defense. Apart from this role, it is involved in numerous non-oxidant processes like biosynthesis of collagen, carnitine, tyrosine and peptide hormones as well as of myelin. It plays the crucial role in neurotransmission and neuronal maturation and functions. For instance, its ability to alleviate seizure severity as well as reduction of seizure-induced damage have been proved. Two basic barriers limit the entry of Vit C (being a hydrophilic molecule) into the central nervous system: the blood-brain barrier and the blood-cerebrospinal fluid barrier (CSF). Considering the whole body, ascorbic acid uptake is mainly conditioned by two sodium-dependent transporters from the SLC23 family, the sodium-dependent Vit C transporter type 1 (SVCT1) and type 2 (SVCT2). These possess similar structure and amino acid  sequence, but  have different tissue distribution. SVCT1 is found predominantly in apical brush-border membranes of intestinal and renal tubular cells, whereas SVCT2 occurs in most tissue  cells .  SVCT2 is especially important for the transport of Vit C in the brain�it mediates the transport of ascorbate from plasma across choroid plexus to the cerebrospinal fluid and across the neuronal cell plasma membrane to neuronal  cytosol .  Although dehydroascorbic acid (DHA) enters the central nervous system more rapidly than the ascorbate, the latter one readily penetrates CNS after oral administration. DHA is taken up by the omnipresent glucose transporters (GLUT), which have affinity to this form of Vit  C .  GLUT1 and GLUT3 are mainly responsible for DHA uptake in the  CNS .  Transport of DHA by GLUT transporter is bidirectional�each molecule of DHA formed inside the cells by oxidation of the ascorbate could be  effluxed  and lost. This phenomenon is prevented by efficient cellular mechanisms of DHA reduction and recycling in ascorbate. Neurons can take up ascorbic acid using both described  ways ,  whereas astrocytes acquire Vit C utilizing only GLUT transporters.

It is well known that the main function of intracellular ascorbic acid in the brain is the antioxidant defense of the cells. However, vitamin C in the central nervous system (CNS) has also many non-antioxidant functions�it plays a role of an enzymatic co-factor participating in biosynthesis of such substances as collagen, carnitine, tyrosine and peptide hormones. It has also been indicated that myelin formation in Schwann cells could be stimulated by ascorbic acid [  7   ,  29   ].

The brain is an organ particularly exposed to oxidative stress and free radicals� activity, which is associated with high levels of unsaturated fatty acids and high cell metabolism rate [  16   ]. Ascorbic acid, being an antioxidant, acts directly by scavenging reactive oxygen and nitrogen species produced during normal cell metabolism [  30   , 31   ]. In vivo studies demonstrated that the ascorbate had the ability to inactivate superoxide radicals�the major byproduct of fast metabolism of mitochondrial neurons [  37  ]. Moreover, the ascorbate is a key factor in the recycling of other antioxidants, e.g., alpha-tocopherol (Vitamin E). Alpha-tocopherol, found in all biological membranes, is involved in preventing lipid peroxidation by removing peroxyl radicals. During this process α-tocopherol is oxidized to the α-  tocopheroxyl  radical, which can result in a very harmful effect. The ascorbate could reduce the  tocopheroxyl  radical back to tocopherol and then its oxidized form is recycled by enzymatic systems with using NADH or NADPH [  33   ]. Regarding these facts, vitamin C is considered to be an important neuroprotective agent.  

One non-antioxidant function of vitamin C is its participation in CNS signal transduction through neurotransmitters [  16   ]. Vit C is suggested to influence this process via modulating of binding of neurotransmitters to receptors as well as regulating their release [  34   ,  35   ,  36   ,  37   ]. In addition, ascorbic acid acts as a co-factor in the synthesis of neurotransmitters, particularly of catecholamines�dopamine and norepinephrine [  26   ,  38   ]. Seitz et al. [  39   ] suggested that the modulating effect of the ascorbate could be divided into short- and long-term ones. The short-term effect refers to ascorbate role as a substrate for dopamine-β-hydroxylase. Vit C supplies electrons for this enzyme catalyzing the formation of norepinephrine from dopamine. Moreover, it may exert neuroprotective influence against ROS and quinones generated by dopamine metabolism [ 16   ]. On the other hand, the long-term effect could be connected with increased expression of the tyrosine hydroxylase gene, probably via a mechanism that entails the increase of intracellular cAMP [  39   ]. It has been stated that the function of ascorbic acid as a neuromodulator of neural transmission may be also associated with amino acidic residues reduction [  40   ] or scavenging of ROS generated in response to neurotransmitter receptor activation [  34   ,  41   ]. Moreover, some have studies showed that ascorbic acid modulates the activity of some receptors such as glutamate as well as γ-aminobutyric acid (GABA) ones [  22   ,  40   ,  42   ,  43   ,  44   ]. Vit C has been shown to prevent excitotoxic damage caused by excessive extracellular glutamate leading to hyperpolarization of the    N  -methyl-  d  -aspartate (NMDA) receptor and therefore to neuronal damage [  45   ]. Vit C inhibits the binding of glutamate to the NMDA receptor, thus demonstrating a direct effect in preventing excessive nerve stimulation exerted by the glutamate [  26   ]. The effect of ascorbic acid on GABA receptors can be explained by a decrease in the energy barrier for GABA activation induced by this agent. Ascorbic acid could bind to or modify one or more sites capable of allosterically modulating single-channel properties. In addition, it is possible that ascorbic acid acts through supporting the conversion from the last GABA-bound closed state to the open state. Alternatively, ascorbic acid could induce the transition of channels towards additional open states in which the receptor adopts lower energy conformations with higher open probabilities [  40   ,  44   ].

There have also been reports concerning the effect of Vit C on cognitive processes such as learning, memory and locomotion, although the exact mechanism of this impact is still being investigated [  26   ]. However, animal studies have shown a clear association between the ascorbate and the cholinergic and dopaminergic systems, they also suggested that the ascorbate can act as a dopamine receptor antagonist. This was also confirmed by Tolbert et al. [  46   ], who showed that the ascorbate inhibits the binding of specific dopamine D1 and D2 receptor agonists.

Another non-antioxidant function of Vit C includes modulation of neuronal metabolism by changing the preference for lactate over glucose as an energy substrate to sustain synaptic activity. During ascorbic acid metabolic switch, this vitamin is released from glial cells and is taken up by neurons where  it  restraints glucose transport and its utilization. This allows lactate uptake and its usage as the primary energy source in neurons [  47   ]. It was observed that intracellular ascorbic acid inhibited neuronal glucose usage via a mechanism involving GLUT3 [  48   ].

Vit C is involved in collagen synthesis, which also occurs in the brain [  26   ]. There is no doubt that collagen is needed for blood vessels and neural sheath formation. It is well recognized that vitamin C takes part in the final step of the formation of mature triple helix collagen. In this stage, ascorbic acid acts as an electron donor in the hydroxylation of procollagen propyl and lysyl residues [  16   ]. The role of Vit C in collagen synthesis in the brain was confirmed by Sotiriou et al. [  49   ]. According to these authors in mice deficient in SVCT2 ascorbate transporter, the concentration of ascorbate in the brain was below detection level. The animals died due to capillary hemorrhage in the penetrating vessels of the brain. Ascorbate-dependent collagen synthesis is also linked to the formation of the myelin sheath that surrounds many nerve fibers [  26   ]. In vitro studies showed that ascorbate, added to a mixed culture of rat Schwann cells and dorsal root ganglion neurons, promoted myelin formation and differentiation of Schwann cells during formation of the basal lamina of the myelin sheath [  7   ,  29   ].

Vit C is important for proper nervous system function and its abnormal concentration in nervous tissue is thought to be accompanied with neurological disorders.    The fact that Vit C can neutralize superoxide radicals, which are generated in large amount during neurodegenerative processes, seems to support its role in neurodegeneration. Moreover, plasma and cellular Vit C levels decline steadily with age and neurodegenerative diseases are often associated with aging. An association of Vit C release with motor activity in central nervous system regions, glutamate-uptake-dependent release of Vit C,  itspossible role in modulation of    N  -methyl-   d   -aspartate receptor activity as well as ability to prevent  peroxynitrite  anion formation constitute further evidence pointing to the role of Vit C in neurodegenerative processes.

Vitamin C is a major antioxidant that protects against oxidative stress and also is known as a neuromodulator in dopaminergic neurons. Adequate levels are required to protect the brain from oxidative stress damage. Lymphocyte vitamin C levels in patients with severe PD were significantly lower (odds ratio [OR], 0.87; 95% confidence interval [CI], 0.80-0.97; P < 0.01) compared with those at less severe stages. Plasma vitamin C levels also tended to be lower in patients with severe PD (4).

 

   There are only a few human studies considering the role of Vit C treatment in PD, the existing ones give some evidences that Vit C treatment may have beneficial effect in PD course. A cohort study involving 1036 PD patients showed that dietary Vit C intake was significantly associated with reduced PD risk. However, it was not significant in a 4-year lagged analysis [   109   ]. Quiroga et al., in turn, reported a case of a 66-year-old man with PD, pleural effusion and bipolar disorder who was found to have low serum Vit C and zinc levels. Intravenous replacement of both Vit C and zinc resulted in resolution of the movement disorder in less than 24 h [   107   ]. The other case report concerned 83-year-old men with dementia, diabetes mellitus, hypertension, benign prostatic hypertension, paroxysmal atrial fibrillation, congestive heart failure and suspected PD. The man was treated with Vit C (200 mg) and zinc (4 mg), which resulted in complete resolution of periungual and gingival bleeding as well as palatal petechiae. Moreover, the man�s orientation and mental status were found to be markedly improved and no further delusions or agitations were observed [   110   ].

The study (2) observations substantiate the previous in vitro findings that ascorbate specifically prevents oxidative degradation of microsomal membranes. The results indicate that vitamin C may exert a powerful protection against degenerative diseases associated with oxidative damage and play a critical role in wellness and health maintenance.

See also  www.myflcv.com/VitCrp.html

 

Other Prevention and Treatment   :

safely replace amalgam fillings(32,33) and detox(  Pectasol  (42), Chlorella(108),  TrueMilkThistle  (55),], [Metals detox:  Pectasol  (42), Quicksilver detox(94), TrueMilkThistle,55;  TrueALA  (55), NAC(52), see doctor(33,89); pesticides: (33,   www.myflcv.com/pesticid.html ), cleanups & cleanses(31) and detox; [other detox:  Pectasol  (42), TrueMilkThistle,detox,55;True ALA, colonics(21), NAC(6,52), Carnosine(52), infra-red sauna]; [  PQQ  (43,51,52,33)- PQQ Improves mitochondrial function, improves cholesterol, improves sleep and moods, cardio function, blood sugar, reduces inflammation(63), People taking PQQ experience  signif  . Decreases in C-Reactive Protein and IL6(markers of inflammation, 64), Mitochondria dysfunction has been implicated in many disease conditions and aging processes (65).]; Super Ubiquinol CoQ10 with PQQ(LE,51), LE Mitochondrial Energy Optimizer with PQQ(51,PQQ, Lipoic Acid, Taurine,  Benfotiamine  , Carnosine (103a), B6) Other T:  Tumeric  Forte with coconut oil/MCT oil(40,2b); (Simvastatin, COQ10,52): [CoQ10 is anti-inflammatory and neuroprotective(103a), clinical trials indicate protection against dementia,  Alz  , etc.)]; [nicotine patch, coffee consumption, COQ10, Fish oil, vit B complex, Vit D3, Carnitine, Green Tea(EGCG),Resveratrol, Curcumin, Melatonin(9), NAC, Lipoic Acid ,52]; Hyperbaric Oxygen Therapy (HBOT)(60b) (HBOT therapy, L-carnitine, Lemon Balm(400mgx3), Dr. Sears(43)), Accel CoQ10,43, Galantamine(improved in 46% of cases), LE( Dec 03) ,      Azilect   (Antiaging ), music therapy, tango ( stretching, balance exercises, tango style walking, footwork patterns, dance with and without partner) ; Tai-chi; coffee and tea suppress; avoid milk; Memantine, 

[  Resveratro  l (prevents acetylation of tau proteins, protects DNA, protects telomeres,108)-red grapes or boiled peanuts]; [lions mane mushrooms (produce nerve growth factor (NGF) (  Amyloban  or lions mane supplements)- prevention or treatment of ALS, 108]; [peppermint tea, curcumin, Gingko biloba, 108]; [divalent copper or copper/zinc balance (108,112)- zinc]

selegiline/  deprenyl  /  cyprenil  ,  Phenylalanine  LE (Sep 03); high iron & manganese associated with  Parkinsons  ; vit D reduces risk of  Parkinsons  , [walking/exercise improves memory,   transdermal nicotine patches   have been found to improve cognitive functioning and other problems in  Parkinsons  patients (52). Blueberries and magnesium reduce oxidative stress and improve cognitive function. Recombinant G-CSF is a possible treatment for  Parkinsons  in clinical trials(52); Physical therapy and exercise beneficial(52), Coffee(52) and tea- but may need periodic abstinence of 2 weeks to sustain effect; [supplements (52): Super Ubiquinol CoQ10 with PQQ(LE,51), Creatine, Fish Oil, complex B  vit;Vit  D3, Carnitine, Green Tea(EGCG), Resveratrol, Curcumin, Melatonin(9), NAC(6), Lipoic Acid] 

Tr: B vitamin group; vitamins E and K& D; and the antioxidant and energetic cofactors alpha-lipoic acid (ALA), ubiquinone (coenzyme Q10; CoQ10), and nicotinamide adenine dinucleotide, reduced (NADH)  

proteolytic enzymes,  TrueEZ  -  D( 55 ), Vit B6, PQQ(51),  UltraAccel  II(PQQ,CoQ10,  vitE  ); 

Balancing neurotransmitters-a usually successful treatment:    (  Hinz  , Shallenberger, 42)-   To learn more about this treatment, and to see a patient�s story, go to  www.youtube.com/thenvcenterantiaging   . Just click on Rod-  Parkinsons  Disease.

Some of causes/factors in  Parkinsons  are similar to   Alzheimers   (  108)- see ICT Protocol and treatments related to sources(108) in Section on  Alzheimers  .

 

Anti-inflammatory Essential Oils   - (eucalyptus, orange, oregano, thieves, chamomile, benzoin, boldo,   camphor ,Citronella  , Helichrysum, Manuka, Mullein, Myrrh, Rosemary, Sage,  Sandelwood  , Spikenard, Tansy,  Vitiver  , Yarrow, combinations, how to use: 22)

 

 

                     References

 

(1)  Does Vitamin C Influence Neurodegenerative Diseases and Psychiatric  Disorders?,   Nutrients  2017 Jul; 9(7): 659. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5537779/

(2)  Vitamin C prevents oxidative damage   , Free  Radic  Res  1996 Aug;25(2):173-9. M K Ghosh et al,  https://pubmed.ncbi.nlm.nih.gov/8885335/

�              ( 3) The International Academy of Oral Medicine and Toxicology, IAOMT,   
The Safe Mercury Amalgam Removal Technique (SMART)

(4) Lymphocyte vitamin C levels as potential biomarker for progression of Parkinson's disease,   Nutrition,  2015 Feb;31(2):406-8. K Ide et al;  https://pubmed.ncbi.nlm.nih.gov/25592020/

(5)   The International Academy of Oral Medicine and Toxicology, IAOMT,   IAOMT Comprehensive Review on Mercury in Dental Amalgam    & 

The International Academy of Oral Medicine and Toxicology, IAOMT,   Mercury Fillings: Dental Amalgam Side Effects and Reactions    &

The International Academy of Oral Medicine and Toxicology, IAOMT,   Mercury Poisoning Symptoms

(6)  N-acetylcysteine (NAC) supplementation increases exercise performance and reduces oxidative stress in individuals with low levels of glutathione   , Free  Radic  Biol Med  2018 Feb 1;115:288-297. V Paschalis et al;  https://pubmed.ncbi.nlm.nih.gov/29233792/

 

(7)    The International Academy of Oral Medicine and Toxicology, IAOMT,   Jawbone Osteonecrosis   ; &    Root Canal Dangers   , Dr, Hal Huggins,    https://iaomt.org/root-canal-dangers/   ; & 

The International Academy of Oral Medicine and Toxicology, IAOMT,    IAOMT     Commentary on the Risks of Root Canal 

(8)  B. Windham, DAMS Intl,  Toxic Metals Connection to Chronic Health Problems   &  Health Effects of Toxic Metals   ; &(c)  Advances in metal-induced oxidative stress and human disease  . Toxicology. 2011 May 10;283(2-3):65-87.  Jomova  K,  Valko   M.;

(9)    High prevalence of extrapyramidal signs and symptoms in a group of Italian dental technicians.  Farbrizio  E et al;   BMC Neurol.    2007 Aug  8;7:24 .

(10)   Uptake of environmental toxicants by the locus  ceruleus  : a potential trigger for neurodegenerative, demyelinating and psychiatric disorders.  Pamphlett   R  ;     Med Hypotheses.    2014 Jan;82(1):97-104; &   Inorganic  mercury in human astrocytes, oligodendrocytes,  corticomotoneurons  and the locus  ceruleus  : implications for multiple sclerosis, neurodegenerative disorders and gliomas.   Pamphlett  R and Kum Jew S;   Biometals   .    2018 Oct;31(5):807-819.

(11)  Accidental Blowup in Medicine, Dr. Simon Yu, 2019 & Accidental Cure, Dr. Simon Yu; & (b) An Unexpected Journey- Searching for a Cause and Finding Hope in the Battle against ALS, Ronald  Unterreiner  , 2019; & � Time to Heal at Last: The Story of Ron�s ALS, Dr. Simon Yu, 2017; & (b) Excitotoxicity is a significant factor in brain inflammation and degeneration, Russell Blaylock, MD; www.russellblaylockmd.com

 (12) a) Dr Russell Blaylock, Wellness Report, Carnitine Compounds Protect against Aging, July 2022, V 19,N 7; &(b) Why is the Incidence of Brain Degeneration Increasing?, Wellness Report, Vol. 20, No.5 & (c) Excitotoxicity is a significant factor in brain inflammation and degeneration, Russell Blaylock, MD; www.russellblaylockmd.com

 

(13)(a) S. Hussain et al, Mercuric chloride‑induced reactive oxygen species and its effect on antioxidant enzymes in different regions of rat  brain,JEnvironSci Health B 1997 May;32(3):395‑409;  &  P.Bulat  , Activity of  Gpx  and SOD in workers occupationally exposed to mercury, Arch  Occup  Environ Health, 1998, Sept, 71 Suppl:S37-9 ; &    Stohs  SJ,  Bagchi  D.  Oxidative mechanisms in the toxicity of metal ions.  Free  Radic  Biol Med 1995; 18(2): 321-36; &  D.Jay  , Glutathione inhibits SOD activity of Hg, Arch Inst  cardiol    Mex, 1998,68(6):457-61; & El-  Demerdash  FM. Effects of selenium and mercury on the enzymatic activities and lipid peroxidation in brain, liver, and blood of rats. J Environ Sci Health B. 2001 Jul;36(4):489-99.  &(b)  S.Tan   et al, Oxidative stress induces programmed cell death in neuronal cells, J  Neurochem  , 1998, 71(1):95-105; & Matsuda T, Takuma K, Lee E, et al.  Apoptosis of  astroglial  cells [Article in Japanese] Nippon  Yakurigaku   Zasshi  . 1998 Oct;112 Suppl 1:24P-; & Lee YW, Ha MS, Kim YK.   Role of reactive oxygen species and glutathione in inorganic mercury-induced injury in human glioma cells.      Neurochem  Res. 2001 Nov;26(11):1187- 93; &  (c)   Ho PI, Ortiz D, Rogers E, Shea TB.    Multiple aspects of homocysteine neurotoxicity: glutamate excitotoxicity, kinase hyperactivation and DNA damage.      J  Neurosci  Res. 2002 Dec 1;70(5):694-702. 

(18)       Kuriane   N, et al;    The effect of different workplace nanoparticles on the immune systems of employees.    J  Nanopart  Res.  2017;19(9):320; & (b) Environmental pollutants as risk factors for neurodegenerative disorders: Alzheimer and Parkinson   diseases.Chin  -Chan M et al;   Front Cell  Neurosci  .   2015 Apr 10;9:124 ; & (c) Neurotoxicity of Metal Mixtures. Andrade et al;    Adv  Neurobiol  .     2017;18:227 -265.

(20) M.  J.Vimy  , Takahashi,Y  ,  Lorscheider,FL  Maternal ‑Fetal Distribution of Mercury Released From Dental Amalgam Fillings. Dept of Medicine and Medical  Physiology , faculty of Medicine, Univ of Calgary, Calgary Alberta Canada, 1990  & Amer.J.Physiol.,1990,  258:R939-945; & (b)   N.D. Boyd,  J.Vimy  , et al,� Mercury from dental "Silver tooth fillings impairs sheep kidney function�,  Am.J  . Physiol. 261 (Regulatory Integrative  Comp   Physiol. 30):R1010‑R1014, 1991.‑  &   (c)       L.Hahn  et al, Distribution of mercury released from  amalgam fillings into monkey tissues,    FASEB J.,1990, 4:5536; &   Galic  N,  Ferencic  Z et al, Dental amalgam  mercury exposure in rats.    Biometals  .  1999 Sep;12(3):227-31.

(27) (a)  Autoimmunity plays a role in Parkinson's disease, study suggests,  Science News, April 20, 2020; &  Gene Variants May Affect PD Risk After Pesticide Exposure, Medscape,  Allergy & Immunology ,  Oct 20, 2020,  https://www.medscape.com/viewarticle/939411#vp_1

&(b) [   Glyphosate exposure exacerbates the dopaminergic neurotoxicity in the mouse brain after repeated administration of MPTP,  Neuroscience Letters   ,  Volume 730   ,   21 June 2020, 135032], & (c )  Association between environmental exposure to pesticides and neurodegenerative diseases   ,  Toxicology and Applied Pharmacology,  Volume 256, Issue 3,       1 November 2011, Pages 379-385.  https://www.sciencedirect.com/science/article/abs/pii/S0041008X1100175X?via%3Dihub  ; & (d )  )   Occupational Exposures and Neurodegenerative Diseases-A Systematic Literature Review and Meta-Analyses  . Int J Environ Res Public Health. 2019 Jan 26;16(3):337. Gunnarsson LG,  Bodin  L. (  Lead ,EMF  ,Pesticides );

(30) (a)Markovich et al, "Heavy metals (Hg, Cd) inhibit the activity of the liver and kidney sulfate transporter Sat‑1",  Toxicol    Appl  Pharmacol  , 1999, 154(2): 181‑7; & (b) 2S.A.McFadden, Xenobiotic metabolism and adverse environmental response: sulfur-dependent detox  pathways,Toxicology  , 1996, 111(1-3):43-65; & (c) S.C. Langley-Evans et al, SO2: a potent  glutathion  depleting agent, Comp  Biochem   PhysiolPharmocol   Toxicol  Endocrinol, 114(2):89-98; &(d)Alberti A,  Pirrone  P, Elia M, Waring RH, Romano C.  Sulphation deficit in low-functioning autistic children. Biol Psychiatry 1999, 46(3):420-4.

(31)  Metals and Parkinson's Disease  : Mechanisms and Biochemical Processes.  Curr  Med Chem. 2018; 25(19):2198-2214. Bjorklund G, Stejskal V, Mutter J. et al; & (b)  Environmental toxins and Parkinson's disease  .  Annu  Rev  Pharmacol   Toxicol  . 2014; 54:141-64. Goldman SM.& (c)  Iron neurochemistry in Alzheimer's disease and Parkinson's disease  : targets for therapeutics. J  Neurochem  . 2016 Oct;139 Suppl 1:179-197.  Belaidi  AA, Bush AI.  & (d)  New Insights on the Role of Manganese in Alzheimer's Disease and Parkinson's Disease.  Int J Environ Res Public Health. 2019 Sep 22;16(19):3546. Martins AC Jr,  Aschner  M.; & (e)  Occupational Exposures and Neurodegenerative Diseases-A Systematic Literature Review and Meta-Analyses  . Int J Environ Res Public Health. 2019 Jan 26;16(3):337. Gunnarsson LG,  Bodin  L.(Lead, EMF, Pesticides); & (f)  Exposure to Pesticides and Welding Hastens the Age-at-Onset of Parkinson's Disease.  Can J Neurol Sci. 2019 Nov;46(6):711-716. ( pesticides , metals) Gamache PL, Dupr � N. et al; & (g)  Neurotoxicity of Metal Mixtures  . Adv  Neurobiol  . 2017; 18:227-265,  Aschner  M et al (synergistic); (h) Disease-Toxicant Interactions in Parkinson's Disease,  Neurochem  Res. 2017 Jun;42(6):1772-1786.  Aschner   M. et al;  Neurochem  Res. 2017 Jun;42(6):1772-1786. & (  i  )  Role of epigenetics in Alzheimer's and Parkinson's disease. Epigenomics . 2010 Oct;2(5):671-82. Kwok JB.

(32)  Detoxification: Heavy Metals Testing and Chelation Therapy-Lyn Patrick, ND (DMSA for challenge test & chelation or MCP) - https://cdn.simplecast.com/audio/4ed1adc9-1b56-4d5d-a2fb-9106997393d4/episodes/6c148e92-bf66-424f-9431-e1a01dbf870d/audio/8773d9e9-9e26-4b2f-aec6-a2004e921e66/default_tc.mp3?aid=rss_feed&feed=1NYUFSRI

& (b)  Take Charge of Your Health (Testing & Chelation of Heavy Metals) - Dr. Chris Shade - CEO of Quicksilver Scientific  https://s115.podbean.com/pb/1860a0ddeed2ad45db31477355f265e8/60103875/data1/fs48/6936790/uploads/Take_Charge_1218208ati1.mp3?pbss=f02615a5-91d0-5c11-8e0e-81cca9f7c721

 

(33)   B. Windham, DAMS, Mercury or metals exposure and health effects,    www.myflcv.com    & Dental Amalgam Mercury Page,  www.myflcv.com/dams.html      (over 5000 peer-reviewed studies cited)

(34)    PatrickStortebecker,Associate   Professor of Neurology, Karolinska Institute, Stockholm.   Mercury Poisoning from Dental amalgam-A Hazard to the Human   Brains   ,  ISBN   : 0-941011001-1& J Canadian Dental Assoc, 33(6): 300-;&   Henriksson  J,  Tjalve  H.  Uptake of inorganic mercury in the olfactory bulbs via olfactory pathways in rats. Environ Res. 1998 May;77(2):130-40.

(35)  Huggins HA,  Levy,TE  ,   Uniformed Consent: the hidden dangers in dental care  , 1999, Hampton Roads Publishing Company Inc; (  Parkinsons  , cavitations , p133)  &  Hal Huggins,   Its   All in Your Head,   1993; & Center for Progressive Medicine, 1999,  other autoimmune conditions (arthritis, diabetes, Lupus,  Parkinsons  , Alzheimer�s , Leukemia, etc. )   http://www.hugginsappliedhealing.com/story3.php   ;�    &    IAOMT,    https://iaomt.org   ; (Safe Amalgam Removal:    https://iaomt.org/for-patients/safe-amalgam-removal/   )

(36)    Epigenetic Factors in Late-Onset Alzheimer's Disease:   MTHFR  and   CTH Gene Polymorphisms, Metabolic  Transsulfuration  and Methylation Pathways, and B Vitamins. Roman GC et al;   Int J Mol Sci.    2019 Jan 14;20(2).

(37)    B. Windham, DAMS, Mercury or metals exposure and health effects,    www.myflcv.com    & Dental Amalgam Mercury Page,  www.myflcv.com/dams.html      (over 5000 peer-reviewed studies cited); & [(b)   Mercury Exposure, Blood Pressure, and Hypertension: A Systematic Review and Dose-response Meta-analysis. Hu XF, Singh K, Chan HM, Environ Health  Perspect  , 2018 July 31 & (c) Low-level exposure to lead, blood pressure, and hypertension in a population-based cohort.  Gambelunghe  A et al, Environ Res. 2016 Aug;149:157-163; & (d) Higher urinary heavy metal, arsenic, and phthalate concentrations in people with high blood pressure  : US NHANES, 2009-2010  . Shiue I;   Blood Press.    2014 Dec;23(6):363-9]

 

(40) Dr. Bruce West, Doctor�s A-Z  Phytoceutical  Guide; & (b) Health Alert, 2017-2019,  http://www.healthalert.com/Articles.aspx

(42)  Rodgers JS,  Hocker  JR, et al, Mercuric ion inhibition of eukaryotic transcription factor binding to DNA.        Biochem   Pharmacol  . 2001 Jun 15;61(12):1543-50; &  Babich    et al, The mediation of mutagenicity and    clastogenicity  of heavy metals by physiochemical factors.  Environ Res., 1985:37;253‑286; & K. Hansen et al A survey of metal induced  mutagenicity  in  vitro and in vivo, J Amer Coll  Toxicol  , 1984:3;381‑430.

(43) (a) Knapp LT;  Klann  E. Superoxide‑induced stimulation of protein kinase C via thiol modification and modulation of zinc content. J Biol Chem 2000 May 22; &  P.Jenner  , Oxidative mechanisms in PD, Mov  Disord  , 1998; 13(Supp1):24-34;&(b)  Rajanna  B et al, Modulation of protein kinase C by heavy metals,  Toxicol  Lett, 1995, 81(2-3):197-203: &  Badou  A et al, HgCl2-induced IL-4 gene expression in T cells involves a protein kinase C-dependent calcium influx through L-type calcium channels J Biol Chem. 1997 Dec 19;272(51):32411-8., &  D.B.Veprintsev  , 1996, Institute for Biological Instrumentation, Russian Academy of Sciences, Pb2+ and Hg2+ binding to alpha‑  lactalbumin.Biochem  Mol Biol Int 1996; 39(6): 1255‑65; & M. J. McCabe, University of Rochester School of Medicine & Dentistry, 2002, Mechanisms of Immunomodulation by Metals, www.envmed.rochester.edu/envmed/TOX/faculty/mccabe.html; &  Buzard GS,  Kasprzak  KS.  Possible roles of nitric oxide and redox cell signaling in metal-induced toxicity and carcinogenesis: a review.  Environ  Pathol   Toxicol  Oncol. 2000;19(3):179-99

(48) Corrosion studies of dental gold alloy in contact with amalgam, Swed. Dent. J 68: 135-139,1984.  K.Arvidson  ,

(49) Kingman A, Albertini T, Brown LJ. National Institute of Dental Research, Mercury concentrations in urine and blood associated with amalgam exposure in the U.S. military population, J Dent Res. 1998 Mar;77(3):461-71.

(52) Life Extension, Disease Prevention and Treatment, Fifth Edition, 2013; &  Life Extension Disease Prevention and Treatment Book, 6th Edition   ; & 

(b)  Life Extension Magazine,    www.lifeextension.com    & Life Extension Magazine, July 2018, etc.

(54)  M.E. Lund et al, Treatment of acute  MeHg  poisoning by NAC, J  Toxicol  Clin  Toxicol  , 1984, 

22(1):31-49; & G. Ferrari et al, Dept. Of Pathology, Columbia Univ., J Neurosci,1995, 15(4):2857-66; & 

RR. Ratan et al, Dept. of Neurology, Johns Hopkins Univ., J  Neurosci  , 1994, 14(7): 4385-92;   Z.Gregus   et al 

Effect of lipoic acid on biliary excretion of glutathione and metals,  Toxicol   APPl   Pharmacol  , 1992, 

114(1):88-96;  &    J.F.  Balch et al, Prescription for Nutritional Healing, 2nd Ed., 1997.        

(56) (a) A. Nicole et al, Direct evidence for glutathione as mediator of apoptosis in neuronal cells, Biomed  Pharmacother  , 1998; 52(9):349-55; & J.P. Spencer et al, Cysteine & GSH in PD, mechanisms involving ROS, J  Neurochem  , 1998, 71(5):2112-22: & J.S. Bains et al, Neurodegenerative disorders in humans and role of glutathione in oxidative stress mediated neuronal death, Brain Res Rev, 1997, 25(3):335-58; &   Antioxidants inhibit the human cortical neuron apoptosis induced by hydrogen peroxide, tumor necrosis factor alpha, dopamine and beta-amyloid peptide 1-42. Free  Radic  Res. 2002 Nov;36(11):1179-84. Medina S,  Hernanz   A ,   &(b) Use of thiols in treatment of PD, Exp Neurol, 1996,141(1):32-9; D.   Offen  et al, & Glutathione elevation and its protective role in acrolein-induced protein damage in  synaptosomal  membranes: relevance to brain lipid peroxidation in neurodegenerative disease.  Neurochem  Int 2001 Aug;39(2):141- 9  ;   Pocernich  CB, et al. & (c) Pearce RK, Marsden CD. Alterations in the distribution of glutathione in the substantia nigra in Parkinson's disease.      J Neural  Transm  . 1997; 104(6-7):661-77; & Ann NY  Acad  Sci, 1996, 786:217-33; A.D. Owen et al, &  Neurochem  Res, 1996, 21(1):35-39;J. J  Heales  et al, & Neurobehavioral effects of NAC conjugates of dopamine: possible relevance for  Parkinsons  Disease,  Chem Res  Toxicol  , 1996, 9(7):1117-26,  X.M.Shen  et al,; & Chem Res  Toxicol  , 1998, 11(7):824-37; & (d)   Brain mitochondria catalyze the oxidation of 7-(2-aminoethyl)-3,4-dihydro-5-hydroxy-2H-1,4-benzothiazine-3-carboxyli c acid (DHBT-1) to intermediates that irreversibly inhibit complex I and scavenge glutathione: potential relevance to the pathogenesis of Parkinson's disease. J  Neurochem  . 1998 Nov;71(5):2049- 62 ;   )        Li H, Shen XM,  Dryhurst  G.  &   ( e)  Mercuric chloride induces apoptosis via a mitochondrial-dependent pathway in human leukemia cells. Toxicology. 2003 Feb 14;184(1):1-9.   Araragi  S, Sato M. et al,

(57)    N.Campbell   &  M.Godfrey,�Confirmation  of Mercury Retention and Toxicity using DMPS   provocation� ,J of Advancement in Medicine, 7(1) 1994;(80 cases);  &(b)  D.Zander  et al,   �Mercury mobilization by DMPS in subjects with and without amalgams�,    Zentralbl   Hyg   Umweltmed  , 1992, 192(5): 447-54(12 cases);

(60)   V.D.  M.Stejskal  , Dept. Of Clinical Chemistry, Karolinska Institute, Stockholm, Sweden          LYMPHOCYTE 

       IMMUNO‑STIMULATION ASSAY ‑MELISA  �  &   VDM Stejskal et al, "MELISA: tool for the study of metal 

       allergy", Toxicology in Vitro, 8(5):991-1000, 1994.

(66)  �Regional brain trace‑element studies in Alzheimer's disease�.   C.MThompson& W.R  .  Markesbery  , et al, Univ. Of Kentucky Dept. Of Chemistry, Neurotoxicology ( 1988  Spring )  9 (1):1‑7 & Hock et al, �Increased blood mercury  levels in  Alzheimer�s  patients�, Neural.    Transm  .    1998,  105 :59-68 & Cornett et al, �Imbalances of trace elements related to oxidative damage in  Alzheimer�s     diseased brain�, Neurotoxicolgy,1998, 19:339-345. 

(67)  A search for longitudinal variations in trace element levels in nails of Alzheimer's disease patients. Vance DE Ehmann WD  Markesbery  WR In: Biol Trace Elem Res (1990 Jul‑Dec)26‑27:461‑70; & Ehmann et al, 1986,  Neurotoxicology ,    7:195-206; &    Thompson et al, 1988, Neurotoxicology, 9:1-7.

 

(84)    J.C.Veltman  et al, �Alterations of heme, cytochrome P-450, and steroid metabolism by mercury in rat adrenal gland�, Arch  Biochem   Biophys  , 1986, 248(2):467-78; &  A.G.Riedl  et al, Neurodegenerative Disease Research Center,  King�s   College,UK  , �P450 and  hemeoxygenase  enzymes in the basal ganglia and their  role�s  in  Parkinson�s  disease�, Adv Neurol, 1999; 80:271-86.

(85)    J. A.Weiner   et  al,�The  relationship between mercury concentration in human organs and predictor variables", Sci Tot Environ, 138(1-3):101-115,1993;  & "An estimation of the uptake of mercury from amalgam fillings in Swedish subjects", Science of the Total Environment, v168,n3, p255-265, 1995.

(92)  L. Tandon et al, "Elemental imbalance studies by INAA on ALS patients", J  Radioanal  Nuclear Chem 195(1):13-19,1995; &     Y.Mano  et al, �Mercury  in the hair of ALS patients�,  Rinsho      Shinkeigaku  , 1989, 29(7): 844-848; & Mano  et al, 1990,  Rinsho   Shinkeigaku  30: 1275-1277; &  Khare  et al, 1990, �Trace  element imbalances in ALS�, Neurotoxicology, 1990,11:521-532.

(94)    F.Berglund  ,   Case reports spanning 150 years on the adverse effects of  dental     amalgam  , Bio-Probe, Inc.,Orlando,Fl,1995;ISBN 0-9410011-14-3(245 cured)

(95)   H.  J.Lichtenberg  , "Elimination of symptoms by removal of dental amalgam from mercury poisoned patients", J  Orthomol  Med 8:145-148, 1993; &         �Symptoms before and after removal of  amalgam�,J   of Orth Med,1996,11(4):195-     (119 cases)

(96)  A. F.Goldberg   et al, �Effect of Amalgam restorations on whole body potassium and bone mineral content in         older  men�,Gen   Dent , 1996, 44(3): 246-8; & K.Schirrmacher,1998, �Effects of lead, mercury, and methyl mercury on gap junctions and [Ca2+]  i  in bone cells�,  Calcif  Tissue Int 1998 Aug;63(2):134‑9. 

(97)  O.  Redhe  et al, "Recovery from ALS after removal of dental amalgam fillings", Int J Risk  &   Safety  in Med 4:229-236, 1994; &  N.Vanacore    et al,  Dirparimento  di  Scienze   Neurologiche  ,      Univer  . La Sapienza, Roma, Med   Lav  (Italy), 1995, Nov, 86(6): 522-533.

(98)   Possible environmental factors for Parkinson's disease ",   A .Seidler   et al, Neurology 46(5): 1275-1284, 1996;  & "Mercury vapor intoxication",  F.O.Vroom  et al,  95: 305-318, 1972; &  �  Parkinsons  Disease and Occupational Exposure to Mercury�, Ohlson et al,   Scand  J. Of Work Environment Health, Vol7, No.4: 252-256, 1981 �  Theraputic  properties of  Unitihiol   � ;  L.G.  Golota,Farm  .  Zh  . 1980, 1: 18- 22;  &   [Parkinsonism in chronic occupational metallic mercury intoxication] Miller K,   Ochudlo  S,   Opala  , et al;  Neurol  Neurochir  Pol. 2003;37 Suppl

(102) R.L.  Siblerud  et  al,"Evidence  that mercury from silver fillings may be an etiological factor in multiple sclerosis", Sci Total Environ,  1994,v 142,n3,     p191- , & �Mental health, amalgam       fillings, and MS�, Psychol Rep,1992, 70(3Pt2), 1139-51; &  T.Engalls,Am  J Forensic Med    Pathol  , 4(1):1983, Mar, 55-61.

(111) (a)  Quig  D, Doctors Data Lab, "Cysteine  metabolism and metal  toxicity", Altern Med Rev,      1998;3:4, p262‑270, & (b)  J.de    Ceaurriz  et al, Role of gamma‑    glutamyltraspeptidase  (GGC) and extracellular      glutathione in dissipation of inorganic  mercury",J  Appl Toxicol,1994, 14(3): 201‑;    & W.O. Berndt et al, "Renal glutathione  and mercury uptake",  Fundam    Appl  Toxicol  , 1985, 5(5):832‑9;   &   Zalups   RK,  Barfuss  DW.   Accumulation and handling of inorganic mercury in the kidney after coadministration with glutathione, J  Toxicol  Environ Health, 1995, 44(4): 385-99; &          T.  W.Clarkson   et al, "  Billiary  secretion of glutathione‑metal complexes",     Fundam  Appl     Toxicol  , 1985,      5(5):816‑31;   

(113) Alzheimer disease: mercury as pathogenetic factor and apolipoprotein E as a moderator.    Neuro Endocrinol Lett.    2004 Oct;25(5):331-9. Mutter J,  Walach  H, et al; & Apolipoprotein E genotyping as a potential biomarker for mercury neurotoxicity.   J  Alzheimers  Dis.   2003 Jun;5(3):189-95, Godfrey ME, Krone CA 

 

(114)   M.Aschner   et al, �Metallothionein induction in fetal rat brain by in utero exposure to elemental mercury           vapor�, Brain Research, 1997, dec 5, 778(1):222-32; &    Aschner    M, Rising L, Mullaney KJ.      Differential sensitivity of neonatal rat astrocyte cultures to mercuric chloride (MC) and methylmercury (  MeHg  ): studies on K+ and amino acid transport and metallothionein (MT) induction.     Neurotoxicology. 1996 Spring;17(1):107-16.  &    T.V.   O�Halloran  , �Transition metals in control of gene expression�, Science, 1993, 261(5122):715-25; & Matts RL, Schatz JR, Hurst R,  Kagen  R.   Toxic heavy metal ions inhibit reduction of disulfide bonds.  J Biol Chem 1991; 266(19): 12695-702; Boot JH.  Effects of SH-blocking compounds on the energy metabolism in isolated rat hepatocytes.  Cell Struct  Funct  1995; 20(3): 233-  8;     &  Baauweegers  HG, Troost D.  Localization of metallothionein in the  mammilian  central nervous  system..     Biol Signals 1994, 3:181-7.      

( 119)( a)    L.Ronnback  et al, "Chronic  encephalopaties  induced by low doses of mercury or lead",   Br J Ind          Med 49: 233-240, 1992; &  H.Langauer‑Lewowicka  ,� Changes in the nervous system due to                         occupational   metallic mercury poisoning� Neurol  Neurochir  Pol 1997 Sep‑Oct;31(5):905‑13; &(b) Kim P, Choi BH.   �Selective inhibition of glutamate uptake by mercury in cultured mouse                      astrocytes�, Yonsei Med J  1995 ;     36(3): 299-305; & Brookes N. In vitro evidence for the role of              glutatmate  in the CNS toxicity of                 mercury.  Toxicology     1992, 76(3):245-56; & Albrecht      J,  Matyja  E.  Glutamate: a potential mediator of    inorganic mercury toxicity.   Metab  Brain Dis 1996;        11:175-84; &   Heavy metals modulate glutamatergic system in human platelets; Borges VC, Santos      FW, Rocha JB, Nogueira CW.   Neurochem     Res. 2007 Jun;32(6):953-8; & Exploration of the direct      metabolic effects of mercury II chloride on      the kidney of Sprague-Dawley rats using high-             resolution magic angle spinning 1H NMR spectroscopy    of intact tissue and pattern recognition;           Wang Y, Bollard ME, Nicholson JK, Holmes E.   J  Pharm   Biomed  Anal. 2006 Feb 13;40(2):375-81; &     Mercury compounds disrupt neuronal glutamate transport in cultured mouse cerebellar granule              cells;      Fonfr�a  E,   Vilar  � MT,   Babot  Z,   Rodr�guez-Farr  � E,  Su�ol  C.       J  Neurosci  Res. 2005 Feb                 15;79(4):545-53

(122)     B.Ono   et al, �Reduced tyrosine uptake in strains sensitive to inorganic mercury�, Genet,                             1987,11(5):399-


(126) (a)   Singh I,  Pahan  K, Khan M, Singh AK. Cytokine-mediated induction of ceramide production is redox-sensitive. Implications to proinflammatory cytokine-mediated apoptosis in demyelinating diseases. J Biol Chem. 1998 Aug 7;273(32):20354-62; &  Pahan  K, Raymond JR, Singh I. Inhibition of phosphatidylinositol 3-kinase induces nitric-oxide synthase in lipopolysaccharide- or cytokine-stimulated C6 glial cells. J. Biol. Chem. 274: 7528-7536, 1999; &Xu J, Yeh CH, et al, Involvement of de novo ceramide biosynthesis in tumor necrosis factor-alpha/cycloheximide-induced cerebral endothelial cell death.  J Biol Chem. 1998 Jun 26;273(26):16521-6; &  Dbaibo  GS, El-  Assaad  W, et  al ,    Ceramide generation by two distinct pathways in tumor necrosis factor alpha-induced cell death.   FEBS Lett. 2001 Aug 10;503(1):7-12; & Liu B,  Hannun  YA.et al, Glutathione regulation of neutral sphingomyelinase in tumor necrosis factor-alpha-induced cell   death .J   Biol Chem. 1998 May 1;273(18):11313-20;       & (b)  Noda M,  Wataha  JC, et al, Sublethal, 2-week exposures of dental material components alter TNF-alpha secretion of THP-1 monocytes.      Dent Mater. 2003 Mar;19(2):101-5; &    Kim SH, Johnson VJ, Sharma RP.    Mercury inhibits nitric oxide production but activates proinflammatory cytokine expression in murine macrophage: differential modulation of NF-  kappaB  and p38 MAPK signaling pathways.    Nitric Oxide. 2002 Aug;7(1):67-74; &   Dastych   J, Metcalfe DD et al,    Murine mast cells exposed to mercuric chloride release granule-associated N-acetyl-beta-D-hexosaminidase and secrete IL-4 and TNF-alpha. J Allergy Clin Immunol. 1999 Jun;103(6):1108- 14  &   ( c)  Tortarolo  M,  Veglianese  P, et al,  Persistent activation of p38 mitogen-activated protein kinase in a mouse model of familial amyotrophic lateral sclerosis correlates with disease progression..  Mol Cell  Neurosci  .  2003 Jun;23(2):180-92.

(139)   G.Sallsten   et al,   �   Mercury in cerebrospinal fluid in subjects exposed to mercury vapor   �   ,  Environmental Research, 1994; 65:195-206.

(142)    Ariza ME;  Bijur  GN; Williams MV.   Lead and mercury mutagenesis: role of H2O 2,  superoxide     dismustase  , and xanthine oxidase.  Environ Mol Mutagen 1998;31(4):352‑ 61  ;   &   M . E.Ariza  et al, Mercury mutagenesis  �   ,  Biochem  Mol  Toxicol  , 1999, 13(2):107-12;  &        M.E.Ariza  et al, 

      Mutagenic effect of mercury",  InVivo  8(4):559-63, 1994;     

 (145)  Carpenter DO.  Effects of metals on the nervous system of humans and animals.        Int J  Occup  Med Environ Health. 2001;14(3):209-18; &    Vanacore   N ,  Bonifati  V, et al  ,  Epidemiology of multiple system atrophy. ESGAP Consortium. European Study Group on Atypical  Parkinsonisms  .  Neurol Sci. 2001 Feb;22(1):97-9; &       J.M.Gorell  et al, �Occupational exposure to mercury, manganese, copper, lead, and the risk of  Parkinson�s  disease�, Neurotoxicology, 1999, 20(2-3):239-47  ;   &     J.M.  Gorell  et al, �Occupational exposures to metals as risk factors for Parkinson's disease�,  Neurology, 1997 Mar, 48:3, 650‑8.  ; &    B.A.Rybicki   et  al,�Parkinson's  disease mortality and the industrial use of heavy metals in Michigan�,  Mov  Disord  , 1993, 8:1, 87‑92.  ; & (b) Chacon Pena JR, Duran  Ferreras  E. Parkinsonism probably induced by manganese] [ Spanish] Rev Neurol. 2001 Sep 1;33(5):434-7; & Chun HS, Lee H, Son JH. Manganese induces endoplasmic reticulum (ER) stress and activates multiple caspases in nigral dopaminergic neuronal cells, SN4741.      Neurosci  Lett. 2001 Dec 4;316(1):5- 8;  &     Discalzi   G,  MeligaF et al; Occupational Mn parkinsonism: magnetic resonance imaging and clinical patterns following CaNa2-EDTA chelation. Neurotoxicology. 2000 Oct;21(5):863-6; &   Brain sites of movement disorder: genetic and environmental agents in neurodevelopmental perturbations.    Neurotox  Res. 2003;5(1-2):1-26   

(147) .   M. Wood, "Mechanisms for the Neurotoxicity of Mercury", in  Organotransitional   Metal   Chemistry, Plenum Publishing Corp, N.Y, N.Y, 1987.

      & R.P. Sharma et al,    �   Metals and Neurotoxic Effects   �   , J of Comp Pathology, Vol 91, 1981.

(148) H.  R.Casdorph  ,   Toxic Metal Syndrome  , Avery Publishing Group, 1995.

(149)  B.Choi  et al, "Abnormal neuronal migration of human fetal brain", Journal of  Neurophalogy  , Vol 37, p719-733, 1978; & F. Monnet- Tschudi  et al,   �   Comparison of the developmental effects of 2 mercury compounds on glial cells and neurons in the rat telencephalon �   , Brain Research, 1996, 741: 52-59; & Chang LW, Hartmann HA,    �   Quantitative cytochemical studies of RNA in experimental mercury poisoning   �   , Acta  Neruopathol  (Berlin), 1973, 23(1):77-83; &  L.Larkfors  et  al,"Methylmercury  induced alterations in the nerve growth factor level in  the developing brain ",  Res Dev Res,62(2),1991,287- ; &(b)   Belletti   S,  Gatti  R.       Time course assessment of methylmercury effects on C6 glioma cells:  submicromolar  concentrations induce oxidative DNA damage and apoptosis.    J  Neurosci  Res. 2002 Dec 1;70(5):703-11.

(158)                Wenstrup et al, �Trace element imbalances in the brains of  Alzheimers  patients�, Research, Vol 533,p125-131,1990; &  F.L.Lorscheider,B.Haley,et  al, �Mercury vapor inhibits tubulin   binding...�, FASEB J,9(4):A-3485.,1995 &   & Vance et al, 1988, Neurotoxicology, 9:197-208; &  de Saint-Georges et al, �Inhibition by mercuric chloride  fo  the in vitro  polymeriztion  of microtubules�, CR Seances Soc Biol Fil, 1984; 178(5):562-6.

(163)  Ahlrot  et al, Nutrition Research, 1985 Supplement, & Second Nordic Symposium on Trace Elements and       Human Health, Odense, Denmark, Aug 1987.


(166)   H.Basun   et al, J Neural  Transm  Park Dis Dement Sect,   �   Metals in plasma and cerebrospinal   fluid in normal aging and Alzheimer �  s disease  �   ,1991,3(4):231-58   .

(169) C.  H.Ngim   et al,  Neuroepidemiology,�Epidemiologic  study on the association between body burden mercury level and idiopathic  Parkinson�sdisease �,  1989, 8(3):128-41.

( 170 ) R . L.Siblerud  ,   �   A  commparison  of mental health of multiple  schlerosis  patients with silver   dental fillings and those with fillings  removed  �   , Psychol Rep, 1992, 70(3),Pt2, 1139-51.

(181) P.W. Mathieson, �Mercury: god of TH2 cells�,1995, Clinical Exp Immunol.,102(2):229-30; & (b)  Heo  Y, Parsons PJ, Lawrence DA, Lead differentially modifies cytokine production in vitro and in vivo.    Toxicol  Appl  Pharmacol  , 196; 138:149-57;

(183) World Health  Organization ( WHO),1991, Environmental Health criteria 118,    Inorgtanic    Mercury, WHO, Geneva; &  Envir  . H. Crit. 101, Methyl Mercury;1990.

 (184)  T. H.Ingalls  , J  Forsenic  Medicine and Pathology, Vol 4, No 1, 1953; & Epidemiology, etiology and prevention of MS  �  ,Am J  Fors  Med & Pathology,  1983, 4:55-61; &   �   Endemic clustering of MS   �   , Am  J.Fors  Med Path, 1986,7:3-8  .

(194)   Lu SC, FASEB J, 1999, 13(10):1169‑ 83,    �   Regulation of hepatic glutathione synthesis:        current concepts and controversies   � ;  & R.B. Parsons, J Hepatol, 1998, 29(4):595-602; &         R.K.Zalups  et  al,"Nephrotoxicity  of inorganic mercury co‑administered with L‑cysteine", Toxicology, 1996, 109(1): 15‑29.  &   T.L. Perry et al,   �   Hallevorden-Spatz   Disease: cysteine accumulation and cysteine dioxygenase  defieciency   �   , Ann Neural, 1985, 18(4):482-489.

(197)   J.Taylor  ,   A Complete Guide to Mercury Toxicity from Dental Fillings   ,Scripps   Pullishing  ;

( 198 )E.S.  West et al, Textbook of Biochemistry, MacMillan Co, 1957,p 853;&       B.R.G.Danielsson   et al,�  Ferotoxicity  of inorganic mercury: distribution and effects of nutrient uptake by placenta and fetus�, Biol Res  Preg  Perinatal. 5(3):102-109,1984; &   Danielsson et al,  Nurotoxicol  .   Teratol  . ,  18 :129-134;

( 204 )Tom  Warren,   Beating  Alzheimer�s   , Avery Publishing Group, 1991.

( 207 )Boyd  Haley, Univ. Of Kentucky � The Toxic Effects  fo  Mercury on CNS Proteins:   Similarity to Observations in  Alzheimer�s  Disease�, IAOMT Symposium paper, March 1997  & �Mercury Vapor  Inhaltion  Inhibits Binding of GTP ...-Similarity to Lesions in  Alzheimers  Diseased Brains�, Neurotoxicology, 18:315- June 1997 &  Met Ions Biol Syst, 1997, 34:461-

( 212 )Ziff , M.F., �Documented Clinical Side Effects to Dental Amalgams�, ADV.  Dent. Res.,1992; 1(6):131-  134;  &     S.Ziff ,  Dentistry   without Mercury  ,  8th Edition, 1996, Bio-Probe, Inc., ISBN 0-941011-04-6; &   Dental Mercury      Detox  , Bio-Probe, Inc.  http://www.bioprobe.com. ( cases:FDA   Patient Adverse Reaction Reports-762,    Dr.M.Hanson  -Swedish patients-519,  Dr. H. Lichtenberg-100 Danish  patients,Dr  .  P.Larose  - 80 Canadian patients,  Dr.  R.Siblerud  , 86 Colorado  patients,Dr  . A.  V.Zamm  , 22 patients)     www.myflcv.com/hgrecovp.html

( 213 )Dr.  C.  Kousmine  ,    Multiple  Scherosis  is Curable  , 1995.

( 221 )R.  Golden et al, Duke Univ., �Dementia and  Alzheimer�s  � Disease�, Minnesota Medicine, 78:p 25-29, 1995.

( 222 )M.    Daunderer ,         Handbuch   der     Amalgamvergiftung  , Ecomed Verlag, Landsberg 1998, ISBN 3‑609‑71750‑5 (in German);   & �Improvement of Nerve and Immunological Damages after Amalgam Removal�, Amer. J. Of Probiotic Dentistry and Medicine, Jan  1991;        & Toxicologische erfahrungen am menchen ; Quecksilber in der umwelf -hearing  zum    amalgamproblem  �   , NiedersachsisclesUmweltministerium , 1991; &   �   Amalgam   �   ,  Ecomed  -Verlag, Landsberg, 1995; &   �   Amalgamtest   �   , Forum  Prakt.Allgen.Arzt  , 1990, 29(8): 213-4; &   �   Besserung   von  Nerven  - und  Immunschaden   nach   Amalgamsanierung   �   ,  Dtsch.Aschr  . F.  BiologischeZahnmedzin  , 1990, 6(4):152-7.   ( amalgam   removal &  DMPS,over  3,000 cases)

( 226 )B.J.    Shenker  et al, Dept. Of   Pathology ,Univ  .  Of Penn. School of Dental Med.,�  Immunotoxic  effects of mercuric compounds on human lymphocytes and  monocytes:Alterations  in cell viability� and   �Immune suppression of   human T-cell activation�,  Immunopharmacologicol     Immunotoxical  , 1992, 14(3):555-77, & 14(3):539-53; & 1993, 15(2-3):273-90;  &   M.A.Miller   et al,    �   Mercuric chloride induces apoptosis in human T lymphocytes   �   ,    Toxicol  Appl  Pharmacol  , 153(2):250‑7 1998   ; & L.M.  Bagentose  et al, �Mercury induced autoimmunity in humans�, Immunol Res, 1999,20(1): 67-78;   &�Mercury-induced autoimmunity�, Clin Exp Immunol, 1998, 114(1):9-12; & Goering PL, Thomas D,  Rojko  JL, Lucas AD.  Mercuric chloride-induced apoptosis is dependent on protein synthesis.    Toxicol  Lett 1999; 105(3): 183-95.

(228) Dr.  Thomas  Rau , Paracelsus  Alergy  Clinic,  Lustmuhle  , Switzerland, 1996, The Swiss Secret to Optimal Health: ( http://www.pbmn.org/inner/rau_interview.html   )

( 229 ) M . Davis,editor  ,   Defense Against Mystery Syndromes�  ,  Chek  Printing Co., &

March,    1994 (case histories documented)

(232) Adolph Coors Foundation, �Coors Amalgam Study: Effects of placement  and   Removal  of Amalgam fillings�, 1995. (www) &  InternationsDAMS Newsletter, p17, Vol VII, Issue 2, Spring 1997. (31 cases)

(233) Sven  Langworth  et  al,�   Amalgamnews   and  Amalgamkadefonden  , 1997 and Svenska Dogbladet,1997 (286 cases); &  F.Berglund,Bjerner /Helm,Klock,Ripa,Lindforss,Mornstad,Ostlin ), �Improved  Health  after Removal of dental  amalgam fillings�, Swedish Assoc. Of Dental  Mercury  Patients  , 1998. (www.tf.nu) (over 1000  cases)    (Sweden has banned amalgam fillings &  Gov�t  maintains health records on all citizens); &(c)   Klock  , B,  Blomgren  , J,  Ripa  , U, Andrup B. Effekt av amalgamavl�gsnande p� patienter som misst�nker att de lider eller har lidit av amalgamf�rgiftning . (Effect of amalgam removal in patients who suspect amalgam poisoning)  Tandl�kartidningen  81, 1989, 1297-1302(198 patients)

(241)   R.Schoeny  , U.S.EPA, �Use of genetic toxicology data in U.S. EPA risk assessment: the mercury study�, Environ Health  Perspect  , 1996, 104, Supp 3: 663-73;   &  C.H.Lee  et al, �Genotoxicity of  phenylHg  acetate in humans as compared to other mercury compounds�, 392(3):269-76.   

(242)   J.Constantinidis   et al, Univ. Of Geneva Medical School, �Hypothesis   regarding amyloid and zinc in the  pathogenisis  of  AlzheiemerDisease �, Alzheimer Dis Assoc   Disord  ,  1991,  5(1):31-35 & G. Bjorklund, �Can  mercury cause  Alzheimer�s  �,  Tidsskr  Nor Laegeforen,1991 

(244)   H.Basun   et al, Dept. Of Geriatric Medicine, Huddinge Hospital, Sweden, �Trace metals in plasma and cerebrospinal fluid in  Alzheimer�sdisease �, J Neural  Transm  Park Dis Dement Sect 1991; 3(4):231-

(248)   Y.Finkelstein   et al, �The enigma of parkinsonism in chronic borderline  mercury intoxication, resolved by challenge with penicillamine.  Neurotoxicology, 1996, Spring, 17(1): 291-5.

(250)      Neuron loss in cerebellar cortex of rats exposed to mercury vapor: a stereological study. Sorensen FW, Larsen JO, et al; Acta  Neuropathol   (  Berl  ). 2000 Jul;100(1):95-100; & ( b)   [ A case of chronic inorganic mercury poisoning with progressive intentional tremor and remarkably prolonged latency of P300]   Shikata  E, Mochizuki Y, et al,   Rinsho   Shinkeigaku  . 1998 Dec;38(12):1064-6.   &(c) �Quantitative analysis of tremor in Minamata disease�,  Yamanaga  H,  Tokhoku  J Exp Med, 1983 Sep, 141:1, 13‑ 22  ; &    (d)Tremor frequency patterns in mercury vapor exposure, compared with early Parkinson's disease and essential tremor.   Biernat  H,  Ellias  SA,  GrandjeanP . Neurotoxicology. 1999 Dec;20(6):945-52; & ( e )Studies  documenting mercury connection to ataxia and tremor,   www.myflcv.com/ataxiaHG.html

(252) B.  J.Shenker   et al, Dept. of Pathology, Univ. of Pennsylvania, �  Immunotoxic  effects of mercuric compounds on human  lymphoctes  and monocytes: Alterations in cellular glutathione content�,  Immunopharmacol   Immunotoxicol  1993, 15(2-3):273-90.

(254) al-Saleh I,  Shinwari  N.  Urinary mercury levels in females: influence of dental amalgam fillings.    Biometals  1997; 10(4): 315-  23;               &  ZabinskiZ ; Dabrowski Z; Moszczynski P; Rutowski J.   The activity of erythrocyte enzymes and basic indices of peripheral  blood   erythrocytes from workers chronically exposed to mercury         vapors.   Toxicol  Ind Health 2000 Feb;16(2):58‑64.

(255)    D.C. Rice, �Evidence of delayed neurotoxicity produced by methyl mercury developmental exposure�, Neurotoxicology, Fall 1996, 17(3-4), p583-96; &    Weiss B, Clarkson TW, Simon W.     Silent  latency    periods in methylmercury poisoning and in neurodegenerative disease.    Environ Health  Perspect  . 2002 Oct;110 Suppl 5:851-4. 

(256) D.  B.Alymbaevaet   al, Med Tr Prom  Ekol  , 6:13-15, 1995 (Russian)

(257)  I. Smith et al, �Pteridines and   mono-amines: relevance to neurological damage�, Postgrad Med J, 62(724): 113-123, 1986; &    A.D.Kayet   al, �Cerebrospinal fluid biopterin is decreased in  Alzheimer�s  disease�,   Arch Neurol, 43(10):  996-9, Oct 1986;   &  T.Yamiguchi  et al, �Effects of  tyrosine  administreation  on serum     bipterin  In patients with  Parkinson�s    Disease and normal controls�, Science, 219(4580):75-77, 1983; &  T.Nagatsu  et al, �  Catecholoamine  -related enzymes and the biopterin cofactor in  Parkinson�s  �, Neurol, 1984, 40: 467-73.

(258)   Clinical Management of Poisoning  , 3rd Ed.,(p753) Haddad, Shannon, and           Winchester, W.B. Sounders and Company,  Philadelphis  , 1998; &   A.D.Kay  et        al, �Cerebrospinal fluid biopterin is decreased in  Alzheimer�s  disease�,        Arch Neurol, 43(10): 996-9, Oct 1986;   &  T.Yamiguchi  et al, �Effects of        tyrosine  administreation  on serum  bipterin  In patients with  Parkinson�s           Disease and normal controls�,  Scinece  , 219(4580):75-77, Jan 1983.


(260) J.S. Woods et al,  �Urinary porphyrin profiles as biomarker of mercury exposure: studies on dentists�, J  Toxicol  Environ Health, 40(2-3):1993, p235-;  & �Altered porphyrin metabolites as a biomarker of mercury exposure and toxicity�,  Physiol  Pharmocol, 1996,74(2):210-15, &   Canadian J Physiology and Pharmacology, Feb 1996;  &  M.D.Martin  et al, �Validity of urine samples for low-level mercury  exposure assessment and relationship to porphyrin and creatinine excretion  rates�, J  Pharmacol  Exp  Ther  , Apr 1996   & J.S. Woods et al, �Effects of  PorphyrinogenicMetals on  Coproporphrinogen  Oxidase in Liver and Kidney� Toxicology and Applied Pharmacology, Vol 97, 183-190, 1989; & (b)  Strubelt  O, Kremer J, et al, Comparative studies on the toxicity of mercury, cadmium, and copper toward the isolated perfused rat liver.  J  Toxicol  Environ Health. 1996 Feb 23;47(3):267-83; &   ( c)  Kaliman  PA,  Nikitchenko  IV, Sokol OA,  Strel'chenko  EV.    Regulation of heme oxygenase activity in rat liver during oxidative stress induced by cobalt chloride and mercury chloride.     Biochemistry (  Mosc  ). 2001 Jan;66(1):77- 82  ; &(d) Kumar SV, Maitra S, Bhattacharya S.        In vitro binding of inorganic mercury to the plasma membrane of rat platelet affects Na+-K+-  Atpase  activity and platelet aggregation.      Biometals  .  2002 Mar;15(1):51-7.

(263)     Kurup   RK,  Kurup  PA.  Hypothalamic digoxin-mediated model for Parkinson's disease.    Int J  Neurosci  . 2003 Apr;113(4):515-36; &     Kumar AR,  Kurup  PA.  Inhibition of membrane Na+-K+ ATPase activity: a common pathway in central nervous system disorders.  J Assoc Physicians India.2002 Mar;50:400- 6;  

(264)    B.R. Danielsson et al,    �       �   Behavioral effects of prenatal metallic mercury inhalation exposure in rats   �   ,  Neurotoxicol   Teratol  , 1993, 15(6): 391- 6;&   A. Fredriksson et al,  �  Prenatal exposure to metallic mercury  vapour  and methylmercury produce interactive behavioral changes in adult rats  �   ,  Neurotoxicol   Teratol  , 1996, 18(2): 129-34;

(271)  B. A.Weber  , �The Marburg Amalgam Study�,  Arzt  und Umwelt, Apr, 1995; (266 cases)  & (b)          B.A. Weber, �Amalgam and Allergy�, Institute for Naturopathic Medicine, 1994;    &      (c)B.A. Weber, �  Conuctivitis  sicca(dry eye study)�,Institute for Naturopathic Medicine, 1994; 

B.A.Weber   ,     �   Alternative  treatment   of  Multiple  Schlerosis  , Tumor,  or  Cancer  �   , Institute  for   Naturopathic  Medicine 1997 (40 MS cases ),               http://home,t‑online.de/home/Institut_f._Naturheilverfahren/patinf.htm"                       

(272)    BJ   Shenker  , Low-level  MeHg  exposure causes human T-cells to undergo apoptosis: evidence of mitochondrial disfunction, Environ Res, 1998, 77(2):149-159; &   Shenker   BJ,  Pankoski  L,  Zekavat  A, Shapiro IM..   Mercury-induced apoptosis in human lymphocytes: caspase activation is linked to redox status.    Antioxid  Redox Signal. 2002 Jun;4(3):379-89.    & Mercuric compounds inhibit human monocyte function by inducing apoptosis: evidence for formation of reactive oxygen species (ROS), development of mitochondrial membrane permeability, and loss of reductive reserve, Toxicology, 1997, 124(3):211-24; O.  Insug   et al, 

(275)    American Journal of Human Genetics,     www.tinyurl.com/68s7j2   , Aug 2008  

(285)  R.C.Perlingeiro  et al, Polymorphonuclear  phagentosis  in workers exposed  to  mercuryvapor  , Int J  Immounopharmacology  , 16(12):1011-7,1994; & Hum Exp  Toxicol  1995, 14(3):281-6;   & M.L. Queiroz et al,  Pharmacol   Toxicol  , 1994, 74(2):72-5; & (b)  J.W.Albers  et al, Neurological abnormalities associated with remote occupational elemental mercury  exposure,Ann  Neurol 1988, 24(5):651-9  ; &    L.Soleo  et al, Effects of low exposure to inorganic mercury on  pyschological  performance, Br J Ind Med, 1990, 47(2):105-9; & (d)  P.J.Smith    et al,   �   Effect of exposure to elemental mercury on short term memory, Br J Ind Med 1983, 40(4):413-9.; & (e)  M.S.Hua  et al,   �   Chronic elemental mercury intoxication   �   , Brain  Inj  , 1996, 10(5):377-84; & (f) Gunther W, et al,  Repeated neurobehavioral investigations in workers ..., Neurotoxicology 1996; 17(3-4):605-14.

( 286 )M.  Lai et al,   Sensiitivity  of MS detections by MRI, Journal of Neurology,  Neruosurgury  , and Psychiatry, 1996, 60(3):339-341.

(288)  (   a)   Hisatome    I,  Kurata  Y, et al;   Block of sodium channels by divalent mercury: role of specific cysteinyl residues in the P-loop region.      Biophys  J. 2000 Sep;79(3):1336- 45;  &   Bhattacharya  S, Sen S et al,   Specific binding of inorganic mercury to Na(+)-K(+)-ATPase in rat liver plasma membrane and signal transduction.       Biometals  .  1997 Jul;10(3):157- 62;      &  Anner  BM,  Moosmayer  M,  Imesch  E.  Mercury blocks Na-K-ATPase by a ligand-dependent and reversible mechanism.   Am J Physiol. 1992 May;262(5 Pt 2 ):F  830-6.     &  Anner  BM,  Moosmayer  M.  Mercury inhibits Na-K-ATPase primarily at the cytoplasmic side.  Am J  Physiol  1992; 262(5 Pt 2 ):F  84308  ;    &    Wagner CA,  Waldegger   S,et   al; Heavy metals inhibit Pi-induced currents through human brush-border NaPi-3 cotransporter in Xenopus oocytes.  .  Am J Physiol. 1996 Oct;271(4 Pt 2 ):F  926-30;    &         Lewis RN; Bowler K.    Rat brain (Na+‑K  +)ATPase  : modulation of its ouabain‑sensitive K+‑  PNPPase  activity by thimerosal. Int J  Biochem  1983;15(1):5‑7  

         & ( b )       Rajanna   B, Hobson M, Harris L, Ware L, Chetty CS.  Effects of cadmium and mercury on  Na( +)- K( +) ATPase and uptake of 3H-dopamine in rat brain synaptosomes.  Arch Int  Physiol   Biochem  1990, 98(5):291-6; &   M .Hobson  ,    B.Rajanna  , �Influence of mercury on uptake of dopamine and norepinephrine�,  Toxicol  Letters, Dep 1985, 27:2-3:7-14;   &        & McKay SJ, Reynolds JN,  Racz  WJ.   Effects of mercury compounds on the spontaneous and potassium-evoked release of [3  H]dopamine   from mouse  striatial  slices.    Can J  Physiol   Pharmacol  1986, 64(12):1507-14;  &   Scheuhammer   AM; Cherian MG.   Effects of heavy metal cations, sulfhydryl reagents and   other chemical agents on striatal D2 dopamine  receptors.Biochem   Pharmacol  1985 Oct 1;34(19):3405‑13   ;&    K.R.Hoyt   et al, �Mechanisms of dopamine-induced cell death and differences from glutamate Induced cell death�, Exp Neurol 1997, 143(2):269-81; &     & (c)  Offen  D, et al, Antibodies from ALS patients inhibit dopamine release mediated by L-type calcium channels.  Neurology 1998 Oct;51(4):1100-3.


(291)    H.A.  Huggins,    Solving the MS Mystery  , 2002,  &   http://www.hugginsappliedhealing.com/ms.php    ; &

  H.  A.Huggins   & TE Levy, �cerebrospinal fluid protein changes in MS  after  Dental amalgam  removal�,   Alternative Med Rev, Aug 1998, 3(4):295-300.

 

 (293)   H.Huggins  ,Burton  Goldberg, & Editors of Alternative Medicine Digest,  Chronic   Fatigue  Fibromyalgia & Environmental Illness  , Future Medicine Publishing, Inc,   1998, p197-;    

  &           CFS,    http://www.hugginsappliedhealing.com/fatigue.php       &        U.Dorffer   , �Anorexia  Hydragyra  : ...�,  Monatsschr  .   Kinderheilkd  . , 1989, 137(8): 472.    

(295) Cecil Textbook of Medicine, 20th Ed., Bennett & Plum, W.B. Saunders and Company, Philadelphia, 1996, p  69;  &   Comprehensive Psychiatry, 18(6), 1977, pp595-598, &  Poisoning & Toxicology Compendium,     Leikin  and  Palouchek  ,   Lexi-Comp., Cleveland, 1998; &  Harrison�s  Principles Of Internal Medicine, 14th Ed., McGraw-Hill,  N.y.  ,   1998.

(296)    L.Bucio   et al, Uptake, cellular distribution and DNA damage produced by mercuric chloride in a human fetal hepatic cell line.    Mutat  Res 1999 Jan 25;423(1‑2):65‑72; & ( b)   Ho PI, Ortiz D, Rogers E, Shea TB.    Multiple aspects of homocysteine neurotoxicity: glutamate excitotoxicity, kinase hyperactivation and DNA 

damage.       J  Neurosci  Res. 2002 Dec 1;70(5):694-702; &(c) Snyder RD;  Lachmann     PJ;  Thiol   involvement in the inhibition of DNA repair by metals in mammalian cells.  Source Mol  Toxicol  , 1989 Apr‑Jun, 2:2, 117‑ 28 ;  &      L.Verschaeve  et al, Comparative in vitro cytogenetic studies in mercury-exposed human lymphocytes�,  Muta  Res, 1985, 157(2-3):221-6;  &  L.  Verschaeve  ,�Genetic damage induced by low level mercury exposure,  Envir  Res,12:306-10,1976. 

(301) Chang  LW ,  Neurotoxic  effects of mercury, Environ. Res.,1977, 14(3):329-73;  &  Histochemical  study on the localization and distribution of mercury in the nervous system after mercury intoxication, Exp Neurol, 1972, 35(1):122-37; & Ultrastructural studies of the nervous system after mercury intoxication,   Acta  Neuropathol  (Berlin), 1972, 20(2):122-38 and 20(4):316-34.

(302) D,  Klinghardt  , IAOMT Conference & tape, 1998; �large study by   M.Daunderer  (Germany) of MS patients after amalgam removal�.

(303)   Heavy Metal and Chemical  Toxicity ,  Dietrich    Klinghardt  , MD, Ph.D.    www.neuraltherapy.com/chemtox.htm    ; & Mercury Toxicity and Systemic Elimination Agents, D.  Klinghardt  & J  Mercola ( DO), J of Nutritional and Environmental Medicine, 2001, 11:53-62; &   Amalgam Detox  ,  Klinghardt  Academy of Neurobiology, 2008  

 

(305) S.  Soederstroem  et al, �The effect of mercury vapor on   chloinergic    neurons in the fetal        brain�,Developmental  Brain Research,85(1):96-108.1995; &   E.M. Abdulla et al,    �   Comparison of neurite outgrowth with neurofilament protein levels In  neuroblastoma cells following mercuric oxide exposure   �   , Clin Exp Pharmocol  Physiol  , 1995, 22(5): 362-3.

( 311 )Chang  LW, Hartmann HA,  �  Blood-brain barrier dysfunction in experimental mercury intoxication  �   .  Acta  Neuropathol   (  Berl  ) 1972;21(3):179-84; & Ware RA, Chang LW, Burkholder PM,    �   An  ultrastructual  study on the blood-brain barrier disfunction following mercury intoxication  �  ,Acta  Neurolpathol  (Berlin), 1974,30(3): 211-214; & Prenatal and neonatal toxicology and pathology of heavy metals  �     Adv  Pharmacol   Chemother ., 1980, 17:195-231.

(313) V.D.  M.Stejskal   et al, Mercury-specific Lymphocytes: an indication of  mercury allergy in  man, J. Of Clinical Immunology, 1996, Vol 16(1);31-40.

( 316 ) B . J.Shenker  et al, Dept. Of Pathology, Univ. Of Pennsylvania School of Dental Medicine, �  Immunotoxic  effects of mercuric compounds on human lymphocytes and monocytes: Alterations in B-cell function and viability�   Immunopharmacol   Immunotoxicol  , 1993, 15(1):87-112; & J.R.Daum  ,�Immunotoxicology of mercury and cadmium on B-lymphocytes�, Int J  Immunopharmacol  ,  1993, 15(3):383-94; &  Johansson U, et al, "The genotype determines the B cell response in mercury-treated mice", Int Arch Allergy Immunol, 116(4):295-305, (Aug 1998) 

(317)   S.Zinecker  , �Amalgam:  Quecksilberdamfe  bis ins  Gehirn  �, der  Kassenarzt  , 1992, 32(4):23;        �  Praxiproblem  Amalgam�, Der  Allgermeinarzt  , 1995,17(11):1215-1221. (1800 patients)

(320) U.  F.Malt   et al, �Physical and mental problems attributed to dental amalgam fillings�, Psychosomatic medicine, 1997, 59:32-41. (99 cured) 

 (322)   P.Engel  , �  Beobachtungen  uber die gesundheit vor und  nach    amalgamentfernug �, Separatdruck aus Schweiz. Monatsschr  Zahnm . 1998, vol 108( 8 ).(  75 cases amalgam removal)   http://soho.globalpoint.ch/paul‑engel

     &    Suspicious dentist now believes patients"     (  Puls  -Tipp, Issue Nov. 2001)

(324) D.  Bangsi  et al, �Dental amalgam and multiple sclerosis�, International J of   Epidemiology, 1998, Aug, 27(4):667-71; & E.  Mauch  et al, � umweltgifte     und  multiple   sklerose  �, Der  Allgremeinarzt  , 1996, 20:2226-2220.

(325)   B.   Arvidson   ( Sweden ), Inorganic mercury is transported from muscular nerve terminals to spinal and brainstem  motorneurons  .  Muscle Nerve, 1992, 15(10);1089-  94,     &  M.  Su  et al, Selective involvement of large motor neurons in the spinal cord of rats treated with methyl mercury.  J Neurol Sci,1998, 156(1):12-7; & Moller, Madsen,  Danscher  , Localization of mercury in CNS of the Rat, Environmental Research, 1986, 41: 29-43.


(326)  E.Baasch  , �Is multiple sclerosis a mercury allergy?�, Schweiz arch Neurol  Neurochir      Psichiatr  , 1966, 98:1-19; & J. Clausen, �Mercury and MS�, Acta Neurol  Scand  , 1993;87:461-; & "Sur un  cas  de  mercurialisme   chronique  simulant la  sclerose   en   plaque",Nord  med Ark Stockholm 1880 xii no 17 1‑48 1 pl  & P. Le Quesne ,�Metal-induced diseases of the nervous system�,1982,Br J Hosp Med,28:534- 

( 327 )a )G.  Danscher  et al, Environ Res, �Localization of mercury in the CNS�, 1986, 41:29-43; &(b)   Danscher  G;  Horsted‑Bindslev  P;  RungbyJ .  Traces of mercury in organs from primates  with   amalgam  fillings.  Exp Mol  Pathol  1990;52(3):291‑9; & (c) �Ultrastructural  localization of mercury after exposure to mercury vapor�, Prog  Histochem      Cytochem  , 1991, 23:249-255; &(d)  Pamphlett   R,Coote  P , �Entry of low doses of mercury vapor into the nervous system�, Neurotoxicology, 1998, 19(1):39-47; & (e)  Pamphlett  et al, �Oxidative damage to nucleic acids in motor neurons containing Hg�, J Neurol Sci,1998,159(2):121-6. (rats & primates); &    ( f)     Pamphlett  R,  Waley  P, "Motor Neuron Uptake of Low Dose Inorganic Mercury",    J. Neurological Sciences 135: 63‑67 (1996); &(g)    Schionning  JD,  Danscher  G, "  Autometallographic  inorganic mercury correlates with  degenerative changes in dorsal root ganglia of rats intoxicated with  organic mercury", APMIS 1999 Mar;107(3):303‑10

(329)  Arvidson    B ; Arvidsson J; Johansson K, "Mercury Deposits in Neurons of the Trigeminal Ganglia After Insertion of Dental Amalgam in Rats",  Biometals  ; 7 (3) p261-263 1994; &  Arvidson  B. Inorganic mercury is transported from muscular nerve  terminasl  to spinal and brainstem  motorneurons .  Muscle Nerve 1992, 15:1089-94;  B.  Arvidson  et al, Acta Neurol  Scand  , �  Retograde  axonal transport of  mercury in primary sensory neurons 1990,82:324-237 &  Neurosci  Letters, 1990, 115:29-32; & S.M.  Candura  et al, Effects of  mercuryic  chloride and  methyly  mercury on cholinergic  neuromusular  transmission,  Pharmacol   Toxicol  1997; 80(5): 218-24; &  Castoldi  AF et al, �Interaction of mercury compounds with muscarinic receptor subtypes in the rat brain�, Neurotoxicology 1996; 17(3-4): 735-41;

(330) (a) Wilkinson LJ, Waring RH.  Cysteine dioxygenase: modulation of expression in human cell lines by cytokines and control of sulphate  production.Toxicol   In Vitro. 2002 Aug;16(4):481-3;; & (b) C.M. Tanner et  al,Abnormal  Liver Enzyme Metabolism in  Parkinsons,Neurology  , 1991, 41(5): Suppl 2, 89-92; &   M.T.Heafield  et al, "Plasma cysteine and sulphate levels in patients with Motor  neurone  disease, Parkinson's Disease, and  Alzheimers  Disease",  Neurosci  Lett, 1990, 110(1‑2), 216,20; &   A.Pean  et al, "Pathways of cysteine metabolism in MND/ALS", J neurol Sci, 1994, 124, Suppl:59‑61;  &  Steventon  GB, et al; Xenobiotic metabolism in motor neuron disease, The Lancet,  Sept 17 1988, p 644-47; & Neurology 1990,   40:1095-98.

(331)     C.Gordon   et al, Abnormal  sulphur  oxidation in systemic lupus (SLE), Lancet, 1992,339:8784,25-6; & Poor  sulphoxidation  in patients with rheumatoid  arthitis  �, Ann Rheum Dis, 1992, 1:3,318-20; P. Emory et al,   & Bradley H, et al, Sulfate metabolism is abnormal in patients with rheumatoid arthritis. Confirmation by in vivo biochemical findings. J  Rheumatol  .  1994 Jul;21(7):1192- 6;   & T.L. Perry et al, et,  Hallevorden-Spatz  Disease: cysteine accumulation and cysteine dioxygenase  defieciency  �, Ann Neural, 1985, 18(4):482-489.

(333)   Effects of Hg2+ and CH3Hg+ on Ca2+ fluxes in the rat brain, Brain Research, 1996, 738(2): 257-64; A.J. Freitas et al, & Inhibition of calcium transport by Hg salts in rat cerebellum and cerebral cortex, J Appl  toxicol  , 1996, 164(4): 325-30; P.R.  Yallapragoda  et al;  &  Mitochondrial calcium release by Hg+2", J Biol Chem, 1988, 263:8, 3582-,  E.Chavez  et al,; Effects of inorganic mercury and methylmercury on the ionic currents of cultured rat hippocampal neurons. Cell Mol  Neurobiol  , 1997,17(3): 273-8 A.  Szucs  et al; & Calcium channels as target sites of heavy metals,  Toxicol  Lett, Dec;82‑83:255‑61 D.  Busselberg  , 1995; & Cell Mol  Neurobiol  1994 Dec;14(6):675‑87; & Modifications of Ca2+ signaling by inorganic mercury in PC12 cells.  FASEB J 1993, 7:1507-14. Rossi AD, et al,

(342)  MELISA: A New Technology for Diagnosing and Monitoring of Metal Sensitivity, Proceedings: 33rd Annual Meeting of American Academy of Environmental Medicine, Nov. 1998, Baltimore, Maryland. V. Stejskal, 

(347) G.  Benga   Water exchange through erythrocyte membranes  ,    Neurol  Neurochir  Pol 1997Sep‑Oct; 31(5):905‑13

(348)  Quecksilbervergiftung   durch  Amalgam: Diagnose und  Therapie   ZWR , 1995,104(5):412-417 A  Kistner  , ; &(b) Maas C, Bruck W.    � Study on the significance of mercury accumulation in the brain from dental amalgam fillings through direct mouth-nose-brain transport,  Zentralbl   Hyg   Umweltmed  1996; 198(3): 275-91; &( c )  Accumulation of mercury in neurosecretory neurons of mice after long-term exposure to oral mercuric chloride.    Neurosci  Lett 1999; 271: 93-96 Villegas J, Crespo D.; & Histochemical changes in the neurosecretory  hypothalic  nuclei as a result of  an intoxication with mercury compounds. Acta  Histochem  Suppl 1980;  22:367-80.  Kozik  MB,  Gramza  G.

(355)   W.Kostler  ,  Beeinflubung der zellularen Immunabwehr drch  Quecksilberfreisetzung  , Forum  Prakt  .   Allgem  .    Arzt  , 1991, 30(2):62-3; & P.Schleicher ,  Schwermetalle schadigen das Immunsystem , Mineraloscope , 1996, (1): 37; &   Immunschaden   durch   Toxine  �   Argumente+Fakten  der  Medizin  , 1992, 05; & W.  Scheicher  , Dissertation,  Universitat  Karlsruhe, 1977.


(363) J.  W.Reinhardt  , Univ. Of Iowa College of Dentistry, �Side effects: mercury contribution to

body burden from dental amalgam�, Adv Dent Res, 1992, 6: 110-3.

(368)  Stejskal VDM,  Danersund  A,  Lindvall  A,  Hudecek  R,  Nordman  V,  Yaqob  A et al.           Metal- specific memory  lymphoctes  : biomarkers of sensitivity in man.  Neuroendocrinology Letters, 1999.

(369)   The beneficial effect of amalgam replacement on health in patients with autoimmunity. Prochazkova  J,  Sterzl  I,  Kucerova H,  Bartova J, Stejskal VD; Neuro Endocrinol Lett. 2004 Jun;25(3):211-8.                                                www.melisa.org/pdf/Mercury-and-autoimmunity.pdf       &

   Sterzl  I,  Prochazkova  J,  Stejaskal  VDM et al, Mercury and nickel allergy: risk  facotrs  in fatigue and       autoimmunity.  Neuroendocrinology Letters 1999; 20:221- 228;  

(372) Atchison WD.  Effects of neurotoxicants on synaptic transmission.   Neuroltoxicol   Teratol     1998;       10(5):393-416.

(376) A multicenter survey of amalgam fillings and subjective complaints in non-selected patients in the dental practice.   Eur J Oral Sci 1998; 106:770-77,  Melchart   D ,  Kremers   L.  (6,744 patients in 34 clinics)

(392)  Gebbart  E.    Chromosone  Damage in Individuals exposed to heavy metals.    Curr  Top Environ  Toxicol  Chem 1985; 8: 213-25.

(400) Fleming L, et al;  Parkinson�s  disease and brain levels of organochlorine  pesticides(  dieldren  ). Annals of Neurology, 1994, 36(1): 100-03; &  Hileman, Bette, "The Environment and Parkinson's," Chemical &   Engineering News, September 17, 2001; & Dopaminergic system modulation, behavioral changes, and oxidative stress after neonatal administration of pyrethroids;   Nasuti  C,   Cantalamessa F    et al;      Toxicology   .    2007 Jan 18;229(3):194-205.   Epub  2006 Oct 29; &   Gesundheitswesen  . 1995 Apr;57(4):214-22; [A new method for early detection of neurotoxic diseases (exemplified by pyrethroid poisoning )]    M�ller-Mohnssen  H, Hahn K; &     Utility of a neurobehavioral screening battery for differentiating the effects of two pyrethroids, permethrin and cypermethrin; McDaniel KL, Moser VC,    Neurotoxicol   Teratol  . 1993 Mar-Apr;15(2):71- 83;    

&   B. Windham, Health Effects of Pesticides, 2001,    www.myflcv.com/pesticid.html

(405)   Jenny Stejskal, Vera Stejskal. The role of metals in autoimmune diseases and the link to neuroendocrinology     Neuroendocrinology Letters, 20:345‑358, 1999.   http://www.melisa.org

(416) (a) Altered metabolism of excitatory amino acids, N-acetyl- aspartate and acetyl-aspartyl-glutamate in amyotrophic lateral sclerosis. Brain Res Bull 1993;30(3-4):381-6,  Plaitakis  A,  Constantakakis  E. & (b) Rothstein JD, Martin LJ,  Kuncl  RW.  Decreased glutamate transport by the brain and spinal cord in ALS.  New  Engl  J Med 1992, 326: 1464-8: & (c) Leigh  Pn  .   Pathologic mechanisms in ALS and other motor neuron diseases. In: Calne DB (Ed.), Neurodegenerative Diseases, WB  Saunder  Co., 1997, p473-88;  &   P .Froissard  et al,  Universite  de Caen, Role of glutathione metabolism in the glutamate-induced programmed cell death of neuronal cells Eur J  Pharmacol  , 1997, 236(1): 93-99; & (d) Kim P, Choi BH. Selective inhibition of glutamate uptake by mercury in cultured mouse astrocytes, Yonsei Med J 1995; 36(3): 299-305; & Brookes N. In vitro evidence for the role of  glutatmate  in the CNS toxicity of mercury.  Toxicology 1992, 76(3):245-56; & Albrecht J,  Matyja  E.  Glutamate: a potential mediator of inorganic mercury toxicity.    Metab  Brain Dis 1996; 11:175-84; &(e) Tirosh O, Sen CK, Roy S, Packer L.  Cellular and mitochondrial changes in  glutamate-induced  HT4 neuronal cell death Neuroscience. 2000;97(3):531- 41;   

(417)  Folkers  K et al, Biochemical evidence for a deficiency of vitamin B6 in subjects reacting to MSL-

        Glutamate.   Biochem   Biophys  Res Comm 1981, 100:   972;     &  Felipo  V et al, L-  carnatine  increases the affinity of glutamate for  quisqualatereceptors and prevents glutamate neurotoxicity. Neurochemical Research 1994, 19(3): 373-377; & Akaike A et al, Protective effects of a vitamin-B12 analog (  methylcobalamin  , against glutamate cytotoxicity in cultured cortical neurons.  European J of Pharmacology 1993, 241(1):1-  6 .

(424) Advanced glycation end products in neurodegeneration: more than early markers of oxidative stress? Ann Neurol 1998 Sep;44(3 Suppl 1): S85‑8. Munch G; Wong A;  Riederer  P.   

(429) (c) Environmental toxins and their common health effects.  Altern Med Rev 2000, 5(3):209-23.  Crinnion  WJ. 

(432) P/Q-type calcium channels mediate the activity-dependent feedback of syntaxin-1A. Nature 1999, 401(6755):800-4; &    Calcium ions in neuronal degeneration;    Wojda   U,   Salinska  E,   Kuznicki  J.      IUBMB Life. 2008 Sep;60(9):575-90

(437) Affinity Labeling Technology, Inc. (Dental Lab), oral toxicity testing technology and tests, see research web pages on amalgam toxicity, root canals,  cavitations .   

(442)  Olanow   CW ,  Arendash  GW. Metals and free radicals in neurodegeneration.   Curr   Opin  Neurol 1994, 7(6):548-58; &  Kasarskis   EJ (MD), Metallothionein in ALS Motor Neurons (IRB #91-22026), FEDRIP DATABASE, National Technical Information Service( NTIS), ID: FEDRIP/1999/07802766.

(443) Down-regulation of copper/zinc superoxide dismutase causes  apototic   dealth  in PC12 neuronal cells. Proc. National  Acad  Sci, USA, 1994, 91(14):6384-7 Troy CM,  Shelanski  ML.; & Chronic inhibition of superoxide dismutase produces apoptotic death of spinal neurons. Proc Nat  Acad   Sci USA, 1994, 91(10):4155-9. Rothstein JD,  Kunci  RW.   

(444) (a) Coenzyme Q10 administration and its potential for treatment of neurodegenerative diseases.    Biofactors  1999, 9(2-4):262-6; Beal MF.  &    DiMauro  S ,  Moses  LG; CoQ10 Use Leads To Dramatic Improvements In Patients With Muscular Disorder,   Neurology, April 2001;& C. Schultz et al, CoQ10 slows progression of  Parkinson�s  Disease; Archives of Neurology, October 15, 2002  & Matthews RT, Yang L, Browne S,  BaikM , Beal MF.  Coenzyme Q10 administration increases brain mitochondrial concentrations and exerts neuroprotective effects.  Proc Natl  Acad  Sci U S A 1998 Jul 21;95(15):8892-7; & Schulz JB, Matthews RT, Henshaw DR, Beal MF.  Neuroprotective strategies for treatment of lesions produced by         

mitochondrial toxins: implications for neurodegenerative diseases.  Neuroscience 1996 Apr;71(4):1043- 8; & Idebenone  - Monograph.  A potent antioxidant and stimulator of nerve growth factor.  Altern Med Rev 2001 Feb;6(1):83-  86;     & (b)Nagano S, Ogawa Y,  Yanaghara  T, Sakoda S.  Benefit of a combined treatment with  trientine  and ascorbate in familial amyotrophic lateral sclerosis model mice.    NeurosciLett   1999,       265(3):159-62;    & (c) C. Gooch et al, Eleanor & Lou Gehrig MDA/ALS Center at Columbia-Presbyterian Medical Center in New York; ALS Newsletter Vol. 6, No. 3 June 2001; & Vitamin Research News, Jan 2008,   www.vrp.com

(462)  Olivieri  G;  Brack  C; Muller‑  Spahn  F;  Stahelin  HB; Herrmann M; Renard  P ;    Brockhaus M; Hock C.        Mercury induces cell cytotoxicity and oxidative stress and increases beta‑amyloid secretion and tau phosphorylation in SHSY5Y neuroblastoma cells.   J  Neurochem  2000 Jan;74(1):231‑6; & (b)  Tabner  BJ, Turnbull S, El-  Agnaf  OM,  Allsop  D.  Formation of hydrogen peroxide and hydroxyl radicals from A(beta) and alpha-synuclein as a possible mechanism of cell death in Alzheimer's disease and Parkinson's disease.  Free  Radic  Biol Med. 2002 Jun 1;32(11):1076-83; &(c) Ho PI, Collins SC, et al; Homocysteine potentiates beta-amyloid neurotoxicity: role of oxidative stress.  J  Neurochem  .  2001 Jul;78(2):249-53. 

( 469)BrainRecovery.com , the book, by  David Perlmutter MD;  Perlmutter Health Center, Naples, Florida,  http://www.perlhealth.com/about.htm; & M.M. van  Benschoten  , Acupoint Energetics of Mercury Toxicity and Amalgam Removal with Case Studies,�� American Journal of Acupuncture, Vol. 22, No. 3, 1994, pp. 251-262; &  M.M. Van  Benschoten    and Associates, Reseda, Calif.  Clinic,   http://www.mmvbs.com/mercury.html

 (477)    Copper in society and the Environment   , Lars  Landner  and Lennart  Lindestrom  .   Swedish Environmental Research  Group ( MFG),2nd revised edition. 1999; &   Neurotoxicity from glutathione depletion is dependent on extracellular trace copper. White AR,  Cappai  R, J  Neurosci  Res. 2003 Mar 15;71(6):889-97; & (c) PARK2 patient  neuroprogenitors  show increased mitochondrial sensitivity to copper.  Aboud  AA et al;   Neurobiol   Dis.    2015 Jan;73:204 -12

(490)    a)    Analysis of SOD1 mutations in a Chinese population with amyotrophic lateral sclerosis: a case-control study and literature review. Wei Q et al;    Sci Rep.    2017 Mar 14;7; &(b) Longitudinal assessment of metal concentrations and copper isotope ratios in the G93A SOD1 mouse model of amyotrophic lateral sclerosis.  Enge  TG et al;   Metallomics   .    2017 Feb 22;9(2):161-174; & ( c ) Resveratrol treatment reduces the vulnerability of SH-SY5Y cells and cortical neurons overexpressing SOD1-G93A to Thimerosal toxicity through SIRT1/DREAM/PDYN pathway.  Laudati  G et al;   Neurotoxicology.    2018 Nov 29;71:6 -15; &   (d)   Changes in the mitochondrial antioxidant systems in neurodegenerative diseases and acute brain disorders.  Ruszkiewicz  J et al;   Neurochem   Int.    2015 Sep;88:66-72. 

 

(494)    ( a)Kobayashi MS, Han D, Packer L.   Antioxidants and herbal extracts protect HT-4 neuronal cells against glutamate-induced cytotoxicity.     Free  Radic  Res 2000 Feb;32(2):115-24(PMID:  10653482;   &  (b)   Ferrante RJ, Klein AM,  Dedeoglu  A, Beal MF  .   Therapeutic efficacy of EGb761 (Gingko biloba extract) in a transgenic mouse model of amyotrophic lateral sclerosis. J Mol  Neurosci  2001 Aug;17(1):89-96         &   Bridi   R,  Crossetti  FP, Steffen VM, Henriques AT.  The antioxidant activity of standardized extract of Ginkgo biloba (  EGb  761) in rats.      Phytother  Res 2001 Aug;15(5):449-  51   ;     &   (e)Li Y, Liu L, Barger     SW,  Mrak  RE, Griffin WS. Vitamin E suppression of microglial activation is neuroprotective. J  Neurosci  Res 2001 Oct 15;66(2):163- 70  ; & (f)    Multiple Antioxidants in the Prevention and Treatment of  Parkinson�s    Disease,  K.N.  Prasad, W.C. Cole, B. Kumar,    Journal of the American College of Nutrition, Vol. 18, No. 5, 413-423 (1999)

(496)    Mercury-induced toxicity of rat cortical neurons is mediated through N-Methyl-D-Aspartate receptors. Xu F et al;    Mol Brain.    2012 Sep 14;5:30

(497)    The effect of curcumin (turmeric) on   Alzheimer's disease  : An overview, Shrikant Mishra, Kalpana  Palanivelu  , Annals of Indian Academy of Neurology, Vol 11(1): 13-19, 2008; & (b) Baum L, Ng A. Curcumin interaction with copper and iron suggests one possible mechanism of action in Alzheimer's disease animal models. Alzheimer's Dis 2004; 6:367-77; & ( c ) Through metal binding, curcumin protects against lead- and cadmium-induced lipid peroxidation in rat brain homogenates and against lead-induced tissue damage in rat brain. J  Inorg   Biochem     2004;98:266  -75, Daniel S,  Limson  JL,

 

(505)    Canesi   M,  Perbellini  L, Pezzoli G.    Poor metabolization of n-hexane in Parkinson's disease.    J Neurol  2003   May ; 250(5):556-60

(506)       Leistevuo  J,  Pyy  L,  Osterblad     M,     Dental amalgam fillings and the amount of organic mercury in human saliva.  Caries Res 2001 May‑Jun;35(3):163‑6

(507) Appel SH, Beers D,  Siklos  L, Engelhardt JI, Mosier DR.  Calcium: the Darth Vader of ALS.  Amyotroph  Lateral  Scler  Other Motor Neuron Disord2001 Mar;2  Suppl  1 :S 47-54

(517) Earl C, Chantry A, Mohammad N.   Zinc ions stabilize the association of basic protein with brain myelin membranes.  J Neurochem1988; 51:718-24; & Riccio P,  Giovanneli  S,  Bobba  A.  Specificity of zinc binding to myelin basic protein.    Neurochem  Res 1995; 20: 1107-13; & Sanders B.  The role of general and metal-specific cellular responses in protection and repair of metal-induced damage: stress proteins and  metallothioneins  .   In:   ChangL   ( Ed. ), Toxicology of Metals. Lewis Publishers, CRC Press Inc, 1996, p835-52; & Mendez-Alvarez E, Soto-Otero R, et  al ,    Effects of aluminum and zinc on the oxidative stress caused by 6-hydroxydopamine autoxidation: relevance for the pathogenesis of Parkinson's disease.      Biochim   Biophys  Acta. 2002 Mar 16;1586(2):155-68.

(518) ( a)    Aluminum deposition in the central nervous system tissues of patients with Parkinson's disease]      [Article in Japanese ] ;   Yasui  M,   Kihira  T, Ota K,   Mukoyama  M, Adachi K.    Rinsho   Shinkeigaku  . 1991 Oct;31(10):1095-8       ;   &(b)    Magnesium deficiency over generations in rats with special references to the pathogenesis of the Parkinsonism-dementia complex and amyotrophic lateral sclerosis of Guam;    Oyanagi   K, Kawakami E,   Yasui  M.      et al;       Neuropathology. 2006 Apr;26(2):115-28; &    Low -calcium, high-aluminum diet-induced motor neuron pathology in cynomolgus monkeys;    Garruto   RM, Shankar SK, Yanagihara R, Salazar AM,  Amyx  HL, Gajdusek DC.  Acta  Neuropathol  .  1989;78(2):210-9; [Similarities in calcium and magnesium metabolism between amyotrophic lateral sclerosis and Parkinsonian-dementia and calcification of the spinal cord in the  Kii  Peninsula ALS  focus  ]  [Article in Japanese] ;   Yasui  M, Yoshida M, Tamaki T, Taniguchi Y, Ota K.      No  To     Shinkei  . 1997 Aug;49(8):745-51

(521)  Guermonprez  L,  Ducrocq  C,  Gaudry-Talarmain  YM.  Inhibition of acetylcholine synthesis and tyrosine nitration induced by  peroxynitritearedifferentially  prevented by antioxidants.       Mol  Pharmacol  2001          Oct;60(4):838-46; & (b)  Mahboob M, Shireen KF, Atkinson A, Khan AT.     Lipid peroxidation and antioxidant enzyme activity in different organs of mice exposed to low level of mercury.    J Environ Sci Health B. 2001 Sep;36(5):687-97.     &    Miyamoto K, Nakanishi H, et al, Involvement of enhanced sensitivity of N-methyl-D-aspartate receptors in vulnerability of developing cortical neurons to methylmercury neurotoxicity.    Brain Res. 2001 May 18;901(1-2):252-8; & (c)   Anuradha B, Varalakshmi P.  Protective role of DL-alpha-lipoic acid against mercury-induced neural lipid peroxidation.      Pharmacol  Res. 1999 Jan;39(1):67-80.

(535) K. Sullivan, Evidence Implicating Amalgam in Alzheimer�s  Disease,                          www.bhoffcomp.com/coping/amalgam.html

(557) Psychiatric Disturbances and Toxic Metals, Townsend Letter for Doctor's & Patients April 2002; & Alternative & Complementary Therapies (a magazine for doctors), Aug 2002;  

(560) J.A. Firestone, Occupational Risk Factors for  Parkinson�s  Disease, Dept of Environmental   Health ,    UW School of Public Health, Univ. of Washington, May 2001.

(564)    Uversky   VN, Li J, Fink AL.  Metal-triggered structural transformations, aggregation, and fibrillation of human alpha-synuclein. A possible molecular NK between Parkinson's disease and heavy metal exposure.  J Biol Chem. 2001 Nov 23;276(47):44284-96.  Epub  2001 Sep 11  ; &  Uversky  VN, Li J, Bower K, Fink AL.       Synergistic effects of pesticides and metals on the fibrillation of alpha-synuclein: implications for Parkinson's disease.    Neurotoxicology. 2002 Oct;23(4-5):527-36

(565)        Shaking up the  Salpetriere  : Jean-Martin Charcot and mercury-induced tremor. Goetz CG,   Neurology.    2010 May 25;74(21):1739-42; & (b)  Quantitative analysis of rapid pointing movements in Cree subjects exposed to mercury and in subjects with neurological deficits.  Beuter  A, de Geoffroy A, Edwards R.  Environ Res. 1999 Jan;80(1):50-63. 

(572) ( b )      � Decreased phagocytosis of myelin by macrophages with ALA.    Journal of Neuroimmunology 1998, 92:67-75; &(c) Packer L, Tritschler HJ, Wessel K.  Neuroprotection by the metabolic antioxidant alpha-lipoic acid.     Free  Radic  Biol Med 1997;22(1-2):359-78(PMID: 8958163); & McCarty MF.  Versatile cytoprotective activity of lipoic acid may reflect its ability to activate  signalling  intermediates that trigger the heat-shock and phase II responses. Med Hypotheses 2001 Sep;57(3):313-7   &Whiteman M, Tritschler H, Halliwell B.  Protection against  peroxynitrite  -dependent tyrosine nitration and alpha 1-antiproteinase inactivation by oxidized and reduced lipoic acid. FEBS Lett 1996 Jan 22;379(1):74-6(PMID: 8566234); &   Patrick L.     Mercury toxicity and antioxidants: Part 1: role of glutathione and alpha-lipoic acid in the treatment of mercury toxicity.  Altern Med Rev. 2002 Dec;7(6):456-71.      & (d )   Z .Gregus   et al, �Effect of lipoic acid on biliary excretion of glutathione and metals�,  Toxicol   APPl   Pharmacol  , 1992, 114(1):88-96; 

(573) Toxic Root Canals, Dr. T. Levy,    The Toxic Tooth   ;& Dr. J. Mercola,    Root Canals Linked to Heart Disease and Inflammatory Conditions   ,; &    TOXIC BACTERIA IN TEETH CONTRIBUTES TO ILLNESS THROUGHOUT THE BODY,    &    ROOT CANAL COVERUP   , DR. G.MEINIG DDS; & 

HTTPS://WWW.FOODMATTERS.COM/ARTICLE/ROOT-CANAL-COVER-UP-EXPOSED   : &    WESTON PRICE FINDINGS,    & 

THE ROOTS OF DISEASE, DR. T LEVY, & HIDDEN EPIDEMIC, SILENT ORAL INFECTIONS CAUSE MOST HEART ATTACKS AND BREAST CANCER, DR. T LEVY,2017

(574) Pritchard C. et al, Pollutants appear to be the cause of the huge rise in degenerative neurological conditions. Public Health, Aug 2004.

(580) Life Extension Foundation (MDs),   Disease Prevention and Treatment  , Expanded 4  th   Edition, 2003 ,  http://www.life-enhancement.com/    & Review: Autoimmune Condition Prevention and Treatment,    www.myflcv.com/autoimmD.html

(590)    Combined lithium and valproate treatment delays disease onset, reduces neurological deficits and prolongs survival in an amyotrophic lateral sclerosis mouse model; Feng HL,  Leng  Y, Ma CH, Zhang J, Ren M, Chuang DM.      Neuroscience. 2008 Aug 26;155(3):567-72.  Epub  2008 Jun 21.

 

(591) The interaction of melatonin and its precursors with aluminum, cadmium, copper, iron, lead, and zinc: an adsorptive  voltammetric  study,  Limson  J,  Nyokong  T,  Daya  S., J Pineal Res. 1998 Jan;24(1):15-21

(592) Aluminum Hydroxide: Another Poison Pediatricians Inject in Babies; IMVA,    http://imva.info/index.php/vaccines/aluminum-hydroxide/    ; & (b) �Vaccines Show Sinister Side, March 23,2006,     www.straight.com/content.cfm?id=16717    ;    (c)    Blaylock, Russell. The Blaylock Wellness Report Vol 1, Issue 1; & (d) Cave,  Stephanie,  Mitchell , Deborah, What Your Doctor May Not Tell You About  Children�s  Vaccinations�, Warner Books, 01 September, 2001; & (e) Waly, M. et al Activation of methionine synthase by insulin-like growth factor-1 and dopamine: a target for neurodevelopmental toxins and thimerosal. Department of Pharmaceutical Sciences, Northeastern University. Molecular Psychiatry (2004) 1-13; & (f) Haley, Boyd. Mercury and Thimerosal Toxicity: A Factor in Autism; & (g) Dr.  Fudenberg�s  comments above were from his speech at the NVIC International Vaccine Conference, Arlington VA September, 1997; & (h)    http://www.chinadaily.com.cn/china/2006-03/25/content_552145.htm

(595)     Mercury toxicity presenting as chronic fatigue, memory impairment and depression: Diagnosis, treatment, susceptibility, and outcomes in a New Zealand general practice setting (1994� 2006 ) ,  D.  P. Wojcik,   M. E. Godfrey, D. Christie3 & B. E. Haley,    Neuroendocrinology Letters Volume 27 No. 4 September 2006

(598)    The Blaylock Wellness Report, Inflammatory Conditions, Vol 5, No. 3, Feb 2008, & Food Additives,  What  you eat can kill you, Vol 4, No. 10,   http://www.blaylockreport.com/

*********

(   600 ) B. Windham, Annotated bibliography: Exposure levels and health effects related to mercury/dental amalgam and results of amalgam replacement, 2017; (over 1500 medical study references documenting mechanism of causality of 40 chronic conditions and over 60,000 clinical cases of recovery or significant improvement of these     conditions after amalgam replacement-documented by doctors)                       

www.myflcv.com/amalg6.html      &   www.myflcv.com/hgremove.html

(   601 ) B. Windham, Cognitive and Behavioral Effects of Toxic Metal Exposures, 2014; (over 150 medical study references)    www.myflcv.com/tmlbn.html ;  

(602) The mechanisms by which mercury causes chronic immune and inflammatory conditions, B. Windham(Ed.), 2017,  www.myflcv.com/immunere.html   ; & NHANES III  Screening 35,000 Americans ,    www.myflcv.com/nhanes3.html

(603) B. Windham (Ed.), The environmental effects of dental amalgam affect everyone, 2012,   www.myflcv.com/damspr2f.html

(604) "Health, Hormonal, and Reproductive Effects of Endocrine Disrupting Chemicals" (including mercury), Annotated Bibliography ,2017, B. Windham,

www.myflcv.com/endohg.html          www.myflcv.com/endocrin.html

(605) Mechanisms of mercury release from amalgam dental fillings: vaporization, oral galvanism, and effects of Electromagnetic fields,    www.myflcv.com/galv.html

(606) Developmental and neurological effects of mercury vapor, B. Windham (Ed)

www.myflcv.com/damspr13.html

Note: etc. when it is used in a list of references means that Author knows of several more references supporting the statement, in #600 for example, but  doesn   �  t think them necessary here.

*****************