Alzheimer’s Disease and Other Autoimmune Degenerative Conditionsthe Mercury Connection.        B. Windham (Editor)   


I.             Introduction and Mercury Exposure

Early signs of ALZ (21,52,108) (tingling in fingers or toes, slow, shuffling gait, cramping in arms or legs, trouble with tongue, facial muscles, swallowing, worsening mood/social skills, spatial memory loss, changes in eating and grooming habits, difficulty in depth perception, loss of smell) 

There has been a huge increase in the incidence of degenerative neurological conditions in virtually all Western countries over the last 2 decades (574,580,594). Alzheimer’s disease is the leading cause of dementia in the elderly. The increase in Alzheimer’s and other dementia has been over 300%.   The primary causes appear to be brain inflammation related to increased exposures to toxic pollutants and bad dietary habits, as well as mitochondrial dysfunction, oxidative stress and depletion of neurotransmitters such as acetylcholine (445,574,577,580,594,598,158,etc.).  These appear to be factors in formation of advanced glycation end products (AGEs) and senile plaques of beta-amyloid peptides, hyper-phosphorylation of Tau, and neurofibrillary tangles-as seen in Alzheimer’s patients.  AGEs also result from high glycemic foods and high temperature cooking.        

Mercury is known to be one of the most toxic substances commonly encountered and to be along with lead the toxic substances adversely affecting the largest numbers of people (276).  Mercury in the presence of other metals in the oral environment undergoes galvanic action, causing movement out of amalgam and into the oral mucosa and saliva (174,183,192,436,199). Mercury in solid form is not stable due to its vapor pressure and oral galvanism of mixed metals, so that it evaporates continuously from amalgam fillings in the mouth, being transferred over a period of time to the host (49,79,83,85,183,199,335, etc.). Mercury vapor is lipid soluble and volatile so crosses the blood brain barrier; as does methyl mercury, which results by the bodies conversion from mercury vapor or inorganic mercury (589,33,606).  The daily total exposure of mercury from fillings is from 3 to 1000 micrograms per day, with the average exposure for those with several fillings being above 30 micrograms per day and the average uptake over 7 ug/day (49,183,199,79,83,85,335,603, etc.), with the majority of the rest excreted through the feces and often being over 30 ug/day (79,335,603). Mercury exposure from dental amalgam involves all 3 forms of mercury, with most initial exposure as vapor, some of which is converted to inorganic mercury-with some of this converted to methyl mercury by bacteria in the intestines (589,33,606). Both mercury vapor and methyl mercury readily cross the blood-brain barrier and cause damage to brain cells. The average amount of mercury in the feces of a group with amalgams was over 10 times that of controls (79,603). A 2009 study found that inorganic mercury levels in people have been increasing rapidly in recent years(543b). It used data from the U.S. Centers for Disease Control and Prevention’s National Health Nutrition Examination Survey (NHANES) finding that while inorganic mercury was detected in the blood of 2 percent of women aged 18 to 49 in the 1999-2000 NHANES survey, that level rose to 30 percent of women by 2005-2006. Surveys in all states using hair tests have found dangerous levels of mercury in an average of 22 % of the population, with over 30% in some states like Florida and New York(543c). A large U.S. Centers for Disease Control epidemiological study, NHANES III, found that those with more amalgam fillings (more mercury exposure) have significantly higher levels of chronic health conditions(543a).


Amalgam fillings are the largest source of mercury in most people with daily exposures documented to commonly be above government health guidelines (49,79,183,199,437b,506,594,33,607,217). 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).  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).  


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 (33,601).  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 (594,33,601,577).

Another major source of mercury exposure is vaccines such as flu vaccines which have large amounts of mercury and aluminum, and have been linked to conditions like depression, Parkinson’s, ALS, and dementia(445,585,598). It has been found that vaccines contain adjuvants like aluminum plus mercury thimerosal which overstimulate the immune system and brain, causing high levels of inflammation over long periods of time. There is evidence of a link between the aluminum hydroxide in vaccines, and symptoms associated with Alzheimer’s, Parkinson's, and ALS(585). It has been found that those who get at least 5 flu shots have an increased risk of inflammatory conditions like Alzheimer’s of at least 500%. 

  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(85,33,577,594).  Mercury exposure is cumulative and comes primarily from 4 main sources: mercury amalgam 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. However bacteria, yeasts, and Vitamin B12 methylate inorganic mercury to methyl mercury in the mouth and intestines (607,505) and mercury inhibits functional methylation in the body, a necessary process (504). Developmental and neurological conditions occur at lower levels of exposure from mercury vapor than from inorganic mercury or methyl mercury(606), but all are extremely toxic and some mercury vapor is converted in the body to  methyl mercury(489).  Mercury in amalgam fillings,  because of its low 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 (49,183,199,209,79,99,33), 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 (217,33).   When amalgam fillings are replaced, levels of mercury in the blood, urine, and feces typically rise temporarily but decline between 60 to 85% within 6 to 9 months (79,33.).

      Susceptibility is a major factor in neurological and immune system damage from toxics such as mercury (490,33, 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, lead, arsenic, and cadmium induce Fe, Cu, and Zn dyshomeiostatis which can result in AD, PD, etc.(18c)

Glutathione is produced by methylation that’s 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 and AD. Other causes of hyperhomocysteinemia include aging, nutritional factors, and deficiencies of B vitamins.


II. Cytotoxic, Neurotoxic, and Immunotoxic Effects of Mercury

 Mercury vapor from amalgam readily crosses cell membranes and binds to the -SH (sulphydryl) groups, resulting in inactivation of sulfur processes and blocking of enzyme functions such as cysteine dioxygenase(CDO), sulfite oxidase, and gamma‑glutamyltraspeptidase(GGC) , producing sulfur metabolites with extreme toxicity that the body is unable to properly detoxify(34,110,115,194,258,330,331,333), along with a deficiency in sulfates required for many body functions.    Sulfur is essential in enzymes, hormones, nerve tissue, and red blood cells.  These exist in almost every enzymatic process in the body.  Blocked or inhibited sulfur oxidation at the cellular level has been found in most with many of the chronic degenerative diseases, including Parkinson’s, Alzheimer’s, ALS, MS, lupus, rheumatoid arthritis, MCS, etc (330,331,34,35,56,194, 258), and appears to be a major factor in these conditions.  The deficiency in conjugation and detoxification of sulfur-based toxins in the liver results in toxic metabolites and progressive nerve damage over time (331). Mercury also blocks the metabolic action of manganese and the entry of calcium ions into cytoplasm (333). Oxidative and nitrosative stress (ONS) contributes to the pathogenesis of most brain maladies, and the magnitude of ONS is related to the ability of cellular antioxidants to neutralize the accumulating reactive oxygen and nitrogen species (ROS/RNS). SOD2 and GSH are critical for the cellular antioxidant defense. Variable changes of the expression or activities of one or more of the mitochondrial antioxidant systems have been documented in the brains derived from human patients and/or in animal models of neurodegenerative diseases (Alzheimer's disease, Parkinson's disease), cerebral ischemia, toxic brain cell damage associated with overexposure to mercury or excitotoxins, or hepatic encephalopathy(490c). Oxidative stress and reactive oxygen species (ROS) have also been implicated as major factors in neurological disorders including stroke, PD, Alzheimer’s, ALS, etc. (13,56,84,169,207b,424,442,453,462). A population-based cross-sectional study in Taiwan found those with amalgam fillings had a higher risk of Alzheimer’s than those without amalgam; also studies had shown mercury from amalgam crosses the blood-brain barrier and cause oxidative and apoptotic damage seen in AD, PD, etc. (589).

Programmed cell death(apoptosis) is documented to be a major factor in degenerative neurological conditions like ALS, Alzheimer’s, MS, Parkinson’s, 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,110a), 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(490,496,593), excess free cysteine levels (56d,110a,34,330), excess glutamate toxicity(13b, 416,445,593,598), excess dopamine toxicity (56d,13a), beta-amyloid generation(462), increased calcium influx toxicity (296b,333,416,432,462c,507) and DNA fragmentation(296,42,115,142) and mitochondrial membrane dysfunction (56defg,416,444d).                                                                             The mechanisms by which mercury causes all of these conditions and neuronal apoptosis are documented in this review (often synergistically along with other toxic exposures).

Chronic neurological conditions such as Alzheimer’s appear to be primarily caused by chronic or acute brain inflammation. The brain is very sensitive to inflammation.  Disturbances in metabolic networks: e.g., immuno-inflammatory processes, insulin-glucose homeostasis, adipokine synthesis and secretion, intra-cellular signaling cascades, and mitochondrial respiration have been shown to be major factors in   chronic neurological conditions (592,593,598,56g). Inflammatory chemicals such as mercury, aluminum, and other toxic metals as well as other excitotoxins including MSG and aspartame cause high levels of free radicals, lipid peroxidation, inflammatory cytokines, and oxidative stress in the brain and cardiovascular systems(13,585,593,595-598) Acetylcholine depletion has been found to be a major factor in Alzheimer’s, and aluminum  has been found to inhibit choline transport and reduce neuronal choline acetyltransferase, which can lead to acetylcholine deficiency (580).

        The brain has elaborate protective mechanisms for regulating neurotransmitters such as glutamate, which is the most abundant of all neurotransmitters. When these protective regulatory mechanisms are damaged or affected, chronic neurological conditions such as Alzheimer’s can result (593).   Mercury and other toxic metals inhibit astrocyte function in the brain and CNS (119), causing increased glutamate and calcium related neurotoxicity (119,333,416,496,593). Mercury and increased glutamate activate free radical forming processes like xanthine oxidase which produce oxygen radicals and oxidative neurological damage(142,13).    Nitric oxide related toxicty caused by peroxynitrite formed by the reaction of NO with superoxide anions, which results in nitration of tyrosine residues in neurofilaments and manganese Superoxide Dimustase(SOD) has been found to cause inhibition of the mitochondrial respiratory chain, inhibition of the glutamate transporter, and glutamate-induced neurotoxicity involved in ALS(524,521,56g).  

 These inflammatory processes damage cell structures including DNA, mitochondria, and cell membranes.  They also activate microglia cells in the brain, which control brain inflammation and immunity.  Once activated, the microglia secrete large amounts of neurotoxic substances such as glutamate, an excitotoxin, which adds to inflammation and stimulates the area of the brain associated with anxiety(593,598). Inflammation also disrupts brain neurotransmitters resulting in reduced levels of serotonin, dopamine, and norepinephrine.   Some of the main causes of such disturbances that have been documented  include vaccines, mercury, aluminum, other toxic metals, MSG, aspartame, etc. (585,593,598,33,etc.)

Programmed cell death (apoptosis) is documented to be a major factor in degenerative neurological conditions like ALS, Alzheimer’s, MS, Parkinson’s, etc.  Some of the factors documented to be involved in apoptosis of neurons and immune cells include mitochondrial membrane dysfunction (56bc, 416).  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.  Mercury depletes GSH and damages cellular mitochrondria, which along with the increased lipid peroxidation in protein and DNA oxidation in the brain appears to be major factors in conditions such as autism, Parkinson’s disease, Alzheimer’s, etc. (34,56,416,442,56g). Some prevention and repair of such damage to mitochondria has been documented using pyroquinoline quinine(PQQ) (56g).


Reduced levels of magnesium and zinc are related to metabolic syndrome, insulin resistance, and brain inflammation and are protective against these conditions(595,43).  Mercury and cadmium inhibiting magnesium and zinc levels as well as inhibiting glucose transfer are other mechanisms by which mercury and toxic metals are factors in metabolic syndrome and insulin resistance/diabetes (43,198,338,597).


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 inflamatory and degenerative neurological conditions like ALS, MS, Parkinson’s, rheumatoid arthritis, etc.  Cell signaling mechanisms like sphingolipids are part of the control mechansim for the TNFa apoptosis mechanism(126a,598).  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).

        Mercury’s biochemical damage at the cellular level include DNA damage, inhibition of DNA and RNA synthesis (42,115,142,197,296,392);  alteration of protein structure (34,110,115,194,252,442);  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 (96,198,254,263,264,34,330,331,339,347, 441,442);  induction of free radical formation(13a,43b,54,405,424), depletion of cellular gluthathione(necessary for detoxification processes) (110,126,424), inhibition of glutathione peroxidase enzyme(13a,442), inhibits glutamate uptake(119,416,445), induces peroxynitrite and lipid peroxidation damage(521b), causes abnormal migration of neurons in the cerebral cortex(149),   immune system damage (34,110,194, 226,252,272,316,325,355); and inducement of inflammatory cytokines(126,181).  Homocysteine has been found to facilitate and increase mercury toxicity (19c). 

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 Alzheimer’s cases there was a reduction in serum magnesium and RBC membrane Na(+)-K+ ATPase activity and an elevation in plasma serum digoxin (263).   The activity of all serum free-radical scavenging enzymes, concentration of glutathione, alpha tocopherol, iron binding capacity, and ceruloplasmin decreased significantly in Alzheimer’s, 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 Alzheimer’s (13a,110,288,442,521b,43,56,263etc.)

         Autoimmunity has also been found to be a factor in chronic degenerative autoimmune conditions such as ALS, with genetic susceptibility a major factor in who is affected.     One genetic factor in Hg induced autoimmunity is major histocompatibility complex(MHC) linked.  Both immune cell type Th1 and Th2 cytokine responses are involved in autoimmunity(425c).  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 Alzheimer’s, Parkinson’s, etc. as early as age 40(437b), whereas those with type APOE-2 readily excrete mercury and are less susceptible (437,35).  Those with type APOE-3 are intermediate to the other 2 types.   The incidence of autoimmune conditions have increased to the extent this is now one of the leading causes of death among women(450).   Also when a condition has been initiated and exposure levels decline, autoimmune antibodies also decline in animals or humans(233,234c,60,369,405)

    Mercury has been found in autopsy studies to accumulate in the brain of those with chronic exposures, and levels are directly proportional to the number of amalgam filling surfaces (85,577).  Dozens of studies have documented that exposure to inorganic mercury causes memory loss and memory problems (435,33).  Mercury has been found to cause memory loss by inactivating enzymes necessary for brain cell energy production and proper assembly of the protein tubulin into microtubules(258). In a recent study, mercury at extremely low levels found commonly in those with amalgam fillings was found to disrupt membrane structure and linear growth rates of neurites in most nerve growth cones exposed, causing tubulin/micortubile structure to disintegrate.  The study also found that mercury also interferes with formation of tubulin producing neurofibrillary tangles in the brain similar to those observed in Alzheimers patients(207,462,594), as well as causing neuronal somata to fail to sprout.  The process was found to result in low levels of zinc in the brain(158,43).  There is evidence that certain redox active metal ions including copper and mercury are important in exacerbating and perhaps facilitating Abeta‑mediated oxidative damage and amyloid deposits in Alzheimer's disease(462,488,590,594).   Mercury has also been shown to  induce cell cytotoxicity and oxidative stress and increases beta‑amyloid secretion and tau phosphorylation in  neuroblastoma cells resulting in amyloid plaques which is found in Alzheimer’s patients, and to also cause the formation of the neurofibrilla tangles found in the Alzheimer’s patient brain(462,258).     Mercury and the induced neurofibrillary tangles also appear to produce a functional zinc deficiency in the  of AD sufferers(242), as well as causing reduced lithium levels which is another factor in such diseases.    Lithium protects brain cells against excess glutamate induced excitability and calcium influx (280,416,445,56). These studies clearly implicate mercury as having the ability to cause neurodegeneration in the brain and CNS, at levels of 20 ppb, which is lower than that of many with several amalgam fillings or dental occupational exposure(462).  Researchers at Geriatric and Psychiatric Univ. Clinics in Basel, Switzerland concluded that inorganic mercury appears to be a causative factor in Alzheimer’s and the Swizz Dental Assoc. recommended avoidance of amalgam use in those with neurological disorders(462).  Clinical experience has also found that DMSO has some ability to repair tubulin damage(594).   

  Clinical tests of patients with MND,ALS, Parkinson’s, Alzheimer’s, Lupus(SLE),  rheumatoid arthritis and autism have found that the patients generally have elevated plasma cysteine to sulphate ratios, with the average being 500% higher than controls(330,331,56,34d), and in general being poor sulphur oxidizers.  This means that these patients have insufficient sulfates available to carry out necessary bodily processes and that cysteine levels build up in the brain and CNS to neurotoxic levels.  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(34). Glutathione is produced through the sulphur oxidation side of this process. Low levels of available glutathione have been shown to increase mercury retention and increase toxic effects(110), while high levels of free cysteine have been demonstrated to make toxicity due to inorganic mercury more severe(333,194,56,34d).  Mercury has also been found to play a part in inducing intolerance and neuronal problems through blockage of the P-450 enzymatic process(84,33d).

Mercury also blocks the immune function of magnesium and zinc (198,427,43,38), whose deficiencies are known to cause significant neurological effects (461,463,443). The low Zn levels result in deficient CuZnSuperoxide dismustase (CuZnSOD), which in turn leads to increased levels of superoxide due to toxic metal exposure(443).  Mercury is known to damage or inhibit SOD activity(34,110).   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)(13,254,489,494-496).

Mercury inhibits sulfur ligands in MT and in the case of intestinal cell membranes inactivates MT that normally bind cuprous ions(477), thus allowing buildup of copper to toxic levels in many and malfunction of the Zn/Cu SOD function.  Modern amalgams commonly used in the U.S. have higher levels of copper than the traditional silver amalgams and result in much higher exposure levels to mercury and copper(258). This is a factor in higher incidence of neurodegnerative condidtions like Alzheimer’s.    Exposure to mercury results in changes in  metalloproteincompounds that have genetic effects, having both structural and catalytic effects on gene expression(115,241,296,442,464,477,495).  Some of the processes affected by such MT 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.  

Copper is an essential trace metal which plays a fundamental role in the biochemistry of the nervous system(489,495,464).   Several chronic neurological conditions involving copper metabolic disorders are well documented like Wilson’s Disease and Menkes Disease.  Mutations in the copper/zinc enzyme superoxide dismustase(SOD) have been shown to be a major factor in the motor neuron degeneration in conditions like familial ALS and similar effects on Cu/Zn SOD to be a factor in other conditions such as autism, Alzheimer’s, Parkinson’s, and non-familial ALS(489,495,464,110).  This condition can result in zinc deficient SOD and oxidative damage involving  nitric oxide, peroxynitrite, and lipid peroxidation(495,496,489), which have been found to affect glutamate mediated excitability and apoptosis of nerve cells and effects on mitochondria (416,445,495, 496,119) These effects can be reduced by zinc supplementation(464,495,517), as well as supplementation with antioxidants and nitric oxide-suppressing agents and peroxynitrite scavengers such as Vit C, Vit E, lipoic acid, Coenzyme Q10, carnosine, gingko biloba, N-acetylcysteine, turmeric, etc.(444,464,494,495,469,497). Some of the antioxidants were also found to have protective effects through increasing catalase and SOD action, while reducing lipid peroxidations(494a).  Curcumin as an antioxidant, anti-inflammatory and lipophilic action improves the cognitive functions in patients with AD (497). A growing body of evidence indicates that oxidative stress, free radicals, beta amyloid, cerebral deregulation caused by bio-metal toxicity and abnormal inflammatory reactions contribute to the key event in Alzheimer's disease pathology. Due to various effects of curcumin, such as decreased Beta-amyloid plaques, delayed degradation of neurons, metal-chelation, anti-inflammatory, antioxidant and decreased microglia formation, the overall memory in patients with AD has improved. Ceruloplasmin in plasma can  be similarly affected by copper metabolism disfunction, like SOD function, and is often a factor in neurodegeneration(489).

 Nanoparticles are widely present in the air of workplace environments and affect immune functions, causing different immune responses. A workplace study (18) showed a statistically significant increased level of the pro-inflammatory cytokine TNF-α in serum in both industry exposed groups compared with office workers, as well as a higher level of TNF-α in workers from the woodworking company compared with the metalworking employees. We found an elevated level of IL-6 in the exposed groups as well as an elevated level of IL-8 in the nasal lavage in woodworking employees after work. Thus it is seen that workplace exposures to air nanoparticles can cause increased inflammatory cytokines and inflammatory conditions, which can damage the neurological and immune systems and be a factor in AD & PD.     


Studies showed that metals can induce A-beta aggregation and toxicity and are concentrated in Alzheimer's brain.  There is accumulating evidence that interactions between beta-amyloid and copper, iron, and zinc are associated with the pathophysiology of Alzheimer's disease (AD) (590).  A significant dyshomeostasis of copper, iron, and zinc has been detected, and the mismanagement of these metals induces beta-amyloid precipitation and neurotoxicity. Chelating agents offer a potential therapeutic solution to the neurotoxicity induced by copper and iron dyshomeostasis. Currently, the copper and zinc chelating agents clioquinol and desferroxamine represent a potential therapeutic route that may not only inhibit beta-amyloid neurotoxicity, but may also reverse the accumulation of neocortical beta-amyloid.  There is also evidence that melatonin and curcumin may have beneficial effects on reducing metal toxicity(591,497). Turmeric/curcumin has been found to reduce some of the toxic and inflammatory effects of toxic metals(497,498).


Low levels of mercury and toxic metals have been found to inhibit dihydroteridine reductase, which affects the neural system function by inhibiting  transmitters through its effect on phenylalanine, tyrosine and tryptophan transport into neurons (122,257,289,342,372).   This was found to cause severe impaired amine synthesis and hypokinesis.  Tetrahydrobiopterin, which is essential in production of  neurotransmitters, is significantly decreased in patients with Alzheimer’s’s, Parkinson’s,  MS, and autism. Such patients have abnormal inhibition of neurotransmitter production. 

         Some studies have also found persons with chronic exposure to electromagnetic fields (EMF) or Wi-fi to have higher levels of mercury exposure and excretion(38). Magnetic fields are known to induce current in metals and would increase the effects of galvanism.    Occupational exposure to higher levels of EMF have also been found in many studies to result in much higher risk of chronic degenerative neurological conditions such as ALS(39) and Alzheimer’s Disease(40)   Since EMF causes increased mercury exposure in those with amalgam, and mercury is also known to cause these conditions, again it is not clear the relative importance of the factors since the studies were not controlled for mercury levels or number of amalgam fillings.   Studies have also found a correlation between high levels of aluminum exposure and dementia such as Alzheimer’s (470,580), and concluded based on extensive literature that the neurotoxic effects of aluminium are beyond any doubt, and aluminium as a factor in some AD cannot be discarded (470b). It is well documented that neurological effects of toxics are synergistic.    Flu shots have mercury and aluminum which both are known to accumulate in the brain over time. A study of people who received flu shots regularly found that if an individual had five consecutive flu shots between 1970 and 1980 (the years studied) his/her chances of getting Alzheimer's Disease is ten times higher than if they had one or no shots (475).  

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 Alzheimer’s (66,67,158,166,204, 207, 221,238,242,244,257,300,303,369,444d,462,35,38d) and significantly improve after dental amalgam replacement and dental infection cleanup.     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 (122,257,289,372). This was found to cause severe impaired amine synthesis and hypokinesis. Tetrahydro-biopterin, which is essential in production of neurotransmitters, is significantly decreased in patients with Alzheimer’s, Parkinson’s, and MS. Such patients have abnormal inhibition of neurotransmitter production. (supplements which inhibit breach of the blood brain barrier such as bioflavonoids have been found to slow such neurological damage).


Also mercury binds with cell membranes interfering with sodium and potassium enzyme functions, causing excess membrane permeability, especially in terms of the blood-brain barrier (155,207,311).   Less than 1ppm mercury in the blood stream can impair the blood- brain barrier.   Mercury was also found to accumulate in the mitochondria and interfere with their vital functions, and to inhibit cytochrome C enzymes which affect energy supply to the brain (43,84,232,35).  Persons with the APO-E4 gene form of apolipoprotein E which transports cholesterol in the blood, are especially susceptible to this damage (207,221,346,437,580), while those with APO-E2 which has extra cysteine and is a better mercury scavenger have less damage.The majority have an intermediate form APO-E3.  This appears to be a factor in susceptibility to Alzheimer’s disease, Parkinson’s disease and multiple sclerosis (291). One’s susceptibility can be estimated by testing for this condition.   Repeated exposure to pesticides has also been found to increase Alzheimer's Disease risk (586).

     A major systematic review of all medical studies found on the connection of mercury exposure and Alzheimer’s Disease was recently carried out by MDs and PhDs. (435) Studies were screened according to a pre-defined protocol. The author’s noted that mercury is one of the most toxic substances known to humans and in addition to being widespread in the environment has also been used extensively in vaccinations and dental amalgam.  Studies were screened according to a pre-defined protocol. Most of the studies testing memory in individuals exposed to inorganic mercury (IM), found significant memory deficits. Some autopsy studies found increased mercury levels in brain tissues of AD patients. “In vitro models showed that IM reproduces all pathological changes seen in AD, and in animal models IM produced changes that are similar to those seen in AD. Its high affinity for selenium and selenoproteins suggests that IM may promote neurodegenerative disorders via disruption of redox regulation.”  IM appears to play a role as a co-factor in the development of AD. It appears to also increase the pathological influence of other metals through adverse effects on the blood brain barrier. “Our mechanistic model describes potential causal pathways.  It concludes: “As the single most effective public health primary preventive measure, industrial, and medical usage of mercury should be eliminated as quickly as possible.”

“Earlier research on the biochemical abnormalities of the Alzheimer’s Diseased (AD) brain showed that mercury, and only mercury, at very low levels induced the same biochemical abnormalities when added to normal human brain homogenates or in the brains of rats exposed to mercury vapor.” (435) "Since the brain is more vulnerable to oxidative stress than any other organ, it is not surprising that mercury, which promotes oxidative stress, is an important risk factor for brain disorders." Low levels of inorganic mercury were able to cause AD- typical nerve cell deteriorations in vitro and in animal experiments. Other metals like zinc, aluminum, copper, cadmium, manganese, iron, and chrome are not able to elicit all of these deteriorations in low levels, yet they aggravate the toxic effects of mercury (Hg) (435b). Amalgam consists of approx. 50 % of elementary mercury which becomes a gas at room temperature and is constantly being vaporized and absorbed by the organism. Mercury levels in brain tissues are 2-10 fold higher in individuals with dental amalgam (435b).  The increased AD risk through APO E4 might be caused by its reduced ability to bind heavy metals.


III.       Insulin resistance as a factor in Alzheimer’s


Higher insulin and glucose levels in the blood and deficiency of glucose in brain cells that need it has been found to lead to neurological problems such as Alzheimer’s (580,581). Those with either type I or type II diabetes have been found to be more likely to have other chronic conditions including heart disease, strokes, kidney disease, Alzheimer’s, eye conditions and blindness (580,581).  Diabetes also impacts memory by increasing the risk blood vessels will become obstructed, restricting blood flow to the brain. High blood glucose levels also impact cognition through formation of sugar-related toxins called advanced glycation end products (AGEs).  AGEs have been found to be a factor in aging, diabetes, and Alzheimer’s.  Glycotoxins are formed when sugars interact with proteins and lipids, damaging the structure of proteins and membranes, rendering them less able to carry out their many vital processes. (581). Studies have shown that AGEs are a key factor in cross-linking of harmful beta-amyloid plaques in the brain that are implicated in Alzheimer’s.   As previously documented mercury and aluminum exposure increase insulin resistance and amalgam replacement and detoxification reduce insulin resistance. 

        Inflammation induced by vaccine adjuvants like aluminum and mercury or by excitotoxins like MSG has been found to play a significant role in insulin resistance (type-2 diabetes) and in high levels of LDL cholesterol (597,598,585,593).  Reduced levels of magnesium and zinc are related to metabolic syndrome, insulin resistance, and brain inflammation, and these are protective against these conditions (599,43).  Mercury and cadmium by inhibiting magnesium and zinc levels as well as inhibiting glucose transfer are other mechanisms by which mercury and toxic metals are factors in metabolic syndrome and insulin resistance/diabetes (43,198,338,597). Mercury inhibits production of insulin and is a factor in diabetes and hypoglycemia, with significant reductions in insulin need after replacement of amalgam filings and normalizing of blood sugar(35,502). Iron overload has also been found to be a cause of insulin resistance/type 2 diabetes(582). 


IV. Other causes/factors of Alzheimer’s (108,52,41,43)

chronic inflammation, oxidative stress, mitochondrial dysfunction, toxins(108,41,33), fluoride(41), poor diet (41,52,108,109), high meat and dairy consumption(109), [diabetes (41,108)-eat to prevent], [poor sleep pattern leads to loss of brain plasticity (108)-shut off TV, computers, smartphones at least an hour before bedtime, warm bath-consider epsum salt bath; go to bed at same time each night, if problem with waking up during night, try a small snack of nuts or plain yogurt before bed; early morning sun and exercise(99,108)-see insomnia]; artificial sweeteners/ Aspartame/ etc. contain methanol which converts for formaldehyde(99c); [lyme disease (33,108), In some studies, 13% of those with AD had Creutzfeldt-Jacob spongiform encephalitis(109c). 20 to 40% of US dairy herds were infected with Bovine tuberculosis- a risk factor in human tuberculosis, etc. (100c)] [HSV-1 (108)-treat(lysine, oil of oregano, olive leaf extract, garlic, grapefruit seed extract,zinc, vit C]; [Metabolic Cognitive Syndrome(low insulin and insulin receptors in brain)(type II diabetes and hypoglycemia related): treat to prevent these conditions-avoid high glycemic foods, add coconut oil or MCT oils, 108a]; [low acetylcholine levels(test and detox environmental toxins)- Acacia extract, skullcap extract, EGCG, Chrysin(108)]; [Resveratrol(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 Alz, 108];[peppermint tea, curcumin, Gingko biloba, 108];  alcohol or tobacco(109f); [(mercury (33,108,113,94), divalent copper from plumbing or supplements (112,108), aluminum(33,108); toxic metals cause inflammation, oxidative stress and mitochondrial insufficiency (33,52,105,108,115) and glutamate toxicity, and inflammatory cytokines which are seen as factors in ALZ(33,108,115), , TNFa promotes amyloid-beta buildup(LE, 2-03,52,108) (33)  -weight training and detox (suppress TNFa. IGF-1 reduces A-beta  buildup (13,33,108)];-test and cleanups & detox, Pectasol(42), milk thistle(108), chlorella or chlorophyll or sulphoraphane (108), for aluminum(lithium,108), IV chelation where needed(33,89,108)], [pesticides & air toxics such as magnetite(108); those living close to heavy traffic have higher dementia risk,108(WHO says air pollution is greatest environmental health threat-causing millions of deaths); reduce air pollution, HEPA air purifier in home & office, HEPA filter on vacuum(108)]; Turmeric Forte with coconut oil(41,108),  L-carnitine (2 gm/ day), music therapy, maple syrup extract(108); [AGEs- Excess glucose causes inflammation resulting in advanced glycation end-products (AGEs) and significant adverse health effects such as high blood sugar, insulin resistance, diabetes, cardiovascular disease, kidney disease, and is a factor in dementia/ Alzheimer’s(52b). Highly processed foods and high temp cooking and dry heat cooking (frying, grilling, roasting) or browning of food also produce AGEs.  Benfotiamine and carnosine counteract AGEs(52b) and improve such conditions(52b). High blood sugar and formaldehyde (from digestive processes & pollution sources) destroy cell structure by cross-linking proteins(52b,108).  Formaldehyde is a factor in dementia, diabetes, depresssion, aging damage, DNA damage(52b). Carnosine protects against formaldehyde damage and cross-linking]. Eating soy regularly was found to increase dementia risk, while fermented soy products such as tempe decreased dementia risk (116).  In some studies, 13% of those with AD had Creutzfeldt-Jacob spongiform encephalitis(109c). 20 to 40% of US dairy herds were infected with Bovine tuberculosis- a risk factor in human tuberculosis, etc. (109c)


V. Treatment of Alzheimer’s

    In some cases replacement of amalgam fillings or toxic metals chelation has been found to result in cure or significant improvement in Alzheimer’s patients (204,35,38c). Alzheimer’s patients commonly are found to be deficient in omega 3 fatty acids, vit C, B12, SAMe, vit K, etc. and clinical experience has found supplementing these to be beneficial in some cases (580). A study demonstrated protective effects of methylcobalamin, a vitamin B12 analog, against glutamate- induced neurotoxicity(503), and similarly for iron in those who are iron deficient .  Supplements with clinical experience indicating benefit in many Alzheimer’s/dementia cases include pantothenic acid(B5), vit B12, vit B1, vit B6, Vit E, Ginkgo Biloba, Vit C, Acetyl-L-Carnatine, CoQ10, EFAs(DHA/EPA), N-Acetyl-Cysteine(NAC), SAMe, folate, inositol, melatonin, carnosine (580).  Two treatments shown to be significantly beneficial in the majority of Alzheimer’s patients using the supplement are Huperzine A and Kami-Umtan-To (KUT) (580).   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 (280).  

 Those with vegetarian and fish diets had lower AD incidence (109). Melatonin is protective. Virgin coconut oil increases glutathione levels and is neuroprotective (108,111);  high homocysteine (see HHCY) (treatment: avoid red meat and dairy(109,111), regular exercise, folate, NAC(52), SAMe, Taurine, TMG, vit B12, Bit B2, Bit B6, Zinc, CDP choline, Creatine(111b) DHEA, curcumin(41) : Super-Bio Curcumin(52,4.5*), Terry Naturally Curamin Extra Strength(4.5*), (B complex vit) ALA,  NAC, quercetin , (Coconut oil, berberine, 99);

Natural Antiparasitic treatments: Essential Oils (oregano, galbanum, nutmeg, sandalwood ,tagetes, combinations) 


Alzheimer’s Individualized Combination Therapy(ICT Protocol)- Dr. Bredesen(UCLA Alzheimer’s Center) and Dr. Rothfeld(108d)-

10 simple steps to eliminate Alzheimer’s- test for nutrient deficiencies, hormone imbalances, toxic metals, and other toxicity indications, then

(1)[Reduce inflammation and stabilize Blood Sugar levels: diet that is low in sugars, simple carbohydrates, llow on glycemic index, plenty of good fats- such as Paleo or low carbohydrate Mediterranean Diet, eat dinner early and fast for 12 hours until breakfast; Supplements: Omega-3s(DHA/EPA), turmeric;    

(2) [Optimize hormone balances (proper nutrition, test and bioidentical hormone treatments, stress reduction-daily exercise, yoga, Tai Chi, music, meditation), Supplements: D3, Ashwagandha];

(3)Optimize Antioxidants- Diet: see step 1, organic blueberries, spinach, kale, oranges; Supplements:

Tocotrienols, tocopherols, selenium, vit C, NAC, ALA;

(4) Optimize Gut Health- Diet: see step 1, Supplements: good prebiotic/probiotic;

(5) Plenty of Healthy Fats: avoid trans-fats, saturated fats in moderation, plenty of polyunstaturated and monounsaturated fats such as avocados, olives, seeds, and nuts, (DHA/EPA), coconut oil or MCT oil;

(6) Enhancing Cognitive Performance and NGF levels- Lion’s Mane mushroom or mushrood extract, Bacopa monnieri and citicoline;

(7) Boost Mitochondrial Function- Supplements: PQQ & CoQ10;

(8) Mental and Physical Exercise daily, crossword puzzles, sudoku, bridge game, online mental games,etc.; low impact cardio or strength training daily;

(9) Ensure Nocturnal Oxygenation-  good steep steps daily and test and treat Sleep Apnea where necessary;

(10) Detox Heavy Metals: detox supplement heavy metals urine test, if silver/mercury/amalgam fillings, replace fillings safely and detox(33,94), Pectasol (43,33), chorella(108), milk thistle(108), IV chelation as needed(89,33), consider kidney & liver cleanse (33,52,31,40,etc.)


(5) U.S. Centers for Disease Control(CDC), National Center for Environmental Health , National Report on Human Exposure to Environmental Chemicals, 2001,; 

(13)(a) S.Hussain et al, “Mercuric chloride‑induced reactive oxygen species and its effect on antioxidant enzymes in different regions of rat brain”,J Environ Sci 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  &(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 & Homocysteine, system b0,+ and the renal epithelial transport and toxicity of inorganic mercury, Bridges CC, Zalups RK.  Am J Pathol. 2004 Oct;165(4):1385-94

(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.

(21)  Dr. Frank Shallenberger, Second Opinion, Journal of Natural Health, 2016-2018, &


(31)   Dr. Hulda Clark, The Cure for All Diseases, New Century Press, 2000

(33)  B. Windham, DAMS,  Mercury or metals exposure and health effects, & Dental Amalgam Mercury Page, (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

(34) (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)S.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 glutathione depleting agent”, Comp Biochem Physiol Pharmocol 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.

(35)  Huggins HA, Levy,TE, Uniformed Consent: the hidden dangers in dental care, 1999, Hampton Roads Publishing Company Inc;   &  Hal Huggins, Its All in Your Head, 1997; & Center for Progressive Medicine, 1999,

(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).

(38) F.Schmidt et al, "Mercury in urine of employees exposed to magnetic fields", Tidsskr Nor Laegeforen, 1997, 117(2): 199‑202; & Sheppard AR and EisenbudM., Biological Effects of electric and magnetic fields of extremely low frequency. New York university press. 1977; & Ortendahl T W, Hogstedt P, Holland RP, "Mercury vapor release from dental amalgam in vitro caused by magnetic fields generated by CRT's", Swed Dent J 1991; & (d)Omura, Yoshiaki; Abnormal Deposits of Al, Pb, and Hg in the Brain, Particularly  in the Hippocampus, as One of the Main Causes of Decreased Cerebral Acetylcholine, Electromagnetic Field Hypersensitivity, Pre-Alzheimer's  Disease, and Autism in Children; Acupuncture & Electro-Therapeutics Research, 2000, Vol. 25  Issue 3/4, p230, 3p; &(e) Effect of radiofrequency radiation from Wi-Fi devices on mercury release from amalgam restorations. Paknahad M et al; J Environ Health Sci Eng. 2016 Jul 13;14:12.

&( &Savitz DA; Checkoway H; Loomis DP.   Magnetic field exposure and neurodegenerative disease mortality among electric utility workers. Epidemiology 1998 Jul;9(4):398‑404; & Savitz DA; Loomis DP; Tse CK.    Electrical occupations and neurodegenerative disease: analysis of U.S.  mortality data.Arch Environ Health 1998 Jan‑Feb;53(1):71‑4;   &    Johansen C; Olsen JH.    Mortality from amyotrophic lateral sclerosis, other chronic disorders, and electric shocks among utility workers. Am J Epidemiol 1998 Aug 15;148(4):362‑8; & Davanipour Z; Sobel E; Bowman JD; Qian Z; Will AD.    Amyotrophic lateral sclerosis and occupational exposure to electromagnetic  fields. Bioelectromagnetics 1997;18(1):28‑35.

(40) Sobel E; Dunn M; Davanipour Z; Qian Z; Chui HC.   Elevated risk of Alzheimer's disease among workers with likely   electromagnetic field exposure.  Neurology 1996 ;47(6):1477‑81; & Sobel E, Davanipour Z.   Electromagnetic field exposure may cause increased production of amyloid beta and eventually lead to Alzheimer's disease. Neurology.1996 Dec;47(6):1594‑600; & Sobel E; Davanipour Z; Sulkava R; Erkinjuntti T; Wikstrom J et al; & Occupations with exposure to electromagnetic fields: a possible risk factor for Alzheimer's disease.   Am J Epidemiol 1995 Sep 1;142(5):515‑24.

(41) Dr. Bruce West, Doctor’s A-Z Phytoceutical Guide; & (c) National Health and Nutrition Examination Survey, 2015 (26,000 adults)


(42) 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; & 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. 

(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; &  Offen D, et al;. Antibodies from ALS patients inhibit dopamine release mediated by L-type calcium channels.  Neurology 1998 Oct;51(4):1100-3.  &(b) B.Rajanna et al, “Modulation of protein kinase C by heavy metals”, Toxicol Lett, 1995, 81(2-3):197-203: & A.Badou 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 Aug;39(6):1255‑65; & M. J. McCabe, University of Rochester School of Medicine & Dentistry, 2002, Mechanisms of Immunomodulation by Metals,;

 (49)    A.Kingman et al, National Institute of Dental Research, “Mercury concentrations in urine and blood associated with amalgam exposure in the U.S. military population”, Dent Res, 1998, 77(3):461-71.

(52) Life Extension, Disease Prevention and Treatment, Fifth Edition, 2013; & (b)  Life Extension, Jan 2019; & (c) Dr. S Panda, The Circadian Code, 2018


(54)    M.E. Lund et al, “Treatment of acute MeHg poisoning by NAC”, J Toxicol Clin Toxicol, 1984, 22(1):31-49; &  Livardjani F; Ledig M; Kopp P; Dahlet M; Leroy M; Jaeger A.  Lung and blood superoxide dismustase activity in mercury vapor exposed rats: effect of N‑acetylcysteine treatment. Toxicology 1991 Mar 11;66(3):289‑95.  & 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;   &  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; & Medina S, Martinez M, Hernanz A,   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.  &(b) D. Offen et al, “Use of thiols in treatment of PD”, Exp Neurol, 1996,141(1):32-9; &  Pocernich CB, 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; & (c)  Pearce RK, Owen A, Daniel S, Jenner P, 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; & A.D.Owen et al, Ann NY Acad Sci, 1996, 786:217-33; & JJ Heales et al, Neurochem Res, 1996, 21(1):35-39; &   X.M.Shen et al, Neurobehavioral effects of NAC conjugates of dopamine: possible relevance for Parkinson’sDisease”,  Chem Res Toxicol, 1996, 9(7):1117-26; & Chem Res Toxicol, 1998, 11(7):824-37; & (d)  Li H, Shen XM, Dryhurst G.   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; & (e) Mitochondrial dysfunction and Alzheimer’s Disease, Prog Neuropsychopharmacol Biol Psychiatry, Jul 2010; & (f) Araragi S, Sato M. et al, Mercuric chloride induces apoptosis via mitochondrial-dependent pathway in human leukemia cells. Toxicology. 2003 Feb 14;184(1):1-9; & (g) Rejuvenate your Cells by Growing New Mitochondria, Life Extension, Winter Edition 2010, pp 3-10(reviews many studies)


(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.

(79) L.Bjorkman et al, "Mercury in Saliva and Feces after Removal of Amalgam Fillings", Toxicology and Applied Pharmacology, 1997, 144(1), p156-62; & (b) J Dent Res 75: 38-, IADR Abstract 165, 1996.

(83)       I.Skare et al, Swedish National Board of Occupational Safety and Health, "Human Exposure to Hg          Released from Dental Amalgam Restorations", Archives of Environmental Health 1994; 49(5):384-394. 

(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;

Alfred V. Zamm. Dental Mercury: A Factor that Aggravates and Induces Xenobiotic Intolerance.  J. Orthmol.      Med. v6#2 pp67-77 (1991).

(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; & M.Nylander et al,   "Mercury concentrations in the human brain and kidneys and exposure from amalgam fillings", Swed Dent J 1987; 11:179-187; & D.W.Eggleston et al, Correlation of dental amalgam with mercury in brain tissue. J Prosthet Dent, 1987,58(6),704-7.

(89)  American College for Advancement in Medicine (ACAM) -training courses in chelation, integrative medicine, functional medicine & location assistance for chelation or functional medicine doctors, online at

 or call 1-800-532-3688.

(94) Quicksilver Scientific Natural Detoxification Products,


(96)   Goyer RA, National Institute of Environmental Health Sciences.  Toxic and essential metal interactions.  Annu Rev Nutr 1997; 17:37-50; & Nutrition and metal toxicity.  Am J Clin Nutr 1995; 61(Suppl 3): 646S-   650S; & Goyer RA et al, Environmental Risk Factors for Osteoporosis, Envir Health Perspectives, 1994, 102(4): 390-394; ; & Lindh U, Carlmark B, Gronquist SO, Lindvall A. Metal exposure from amalgam alters the              distribution of trace  elements in blood cells and plasma.  Clin Chem Lab Med 2001 Feb;39(2):134‑142. ; & 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..

(99) Dr. Richard Gerhauser, Natural Health Response , & (b) Secrets of Underground Medicine, 2018; &(c) Dr. Woodrow Montes, A.S.U., While Science Sleeps, a Sweetener Kills,

(100)  (a)The incidence of dementia and intake of animal products: preliminary findings from the Adventist Health Study.  Neuroepidemiology, 1993;12(1):28-36. Giem P et al; &(b) Dietary patterns associated with Alzheimer's disease: a population based study. Gustaw-Rothenberg K et al; Int J Environ Res Public Health. 2009 Apr;6(4):1335-40; & (c) Thinking the unthinkable: Alzheimer's, Creutzfeldt-Jakob and Mad Cow disease: the age-related reemergence of virulent, foodborne, bovine tuberculosis or losing your mind for the sake of a shake or burger. Broxmeyer L et al; Med Hypotheses. 2005;64(4):699-705; & (d) Association between dietary patterns and cognitive function among 70-year-old Japanese elderly: a cross-sectional analysis of the SONIC study. Okubo H et al; Nutr J. 2017 Sep 11;16(1):56; & (e) Relationships of Dietary Patterns, Foods, and Micro- and Macronutrients with Alzheimer's Disease and Late-Life Cognitive Disorders: A Systematic Review. Solfrizzi V et al;
J Alzheimers Dis.
 2017;59(3):815-849; & (f) Chronic Neurodegenerative Illnesses and Epilepsy in Danish Adventists and Baptists: A Nationwide Cohort Study. Thygesen et al.  J Alzheimers Dis.  2017;56(4):1429-1435.


(108) (a) The Complete Guide to Reversing Alzheimer’s, Dr, Glen Rothfeld, & (b)   81 Natural Cures for Cancer, Alzheimer’s, Diabetes, etc.  Dr. Rothfeld, & (c) Dr. Rothfelds Health Secrets for Men, & (d) The End of Alzheimer’s: A Program to Prevent and Reverse Cognitive Decline; Dr. Dale Bredesen(UCLA), Aug 2017

(109) (a)The incidence of dementia and intake of animal products: preliminary findings from the Adventist Health Study.  Neuroepidemiology, 1993;12(1):28-36. Giem P et al; &(b) Dietary patterns associated with Alzheimer's disease: a population based study. Gustaw-Rothenberg K et al; Int J Environ Res Public Health. 2009 Apr;6(4):1335-40; & (c) Thinking the unthinkable: Alzheimer's, Creutzfeldt-Jakob and Mad Cow disease: the age-related reemergence of virulent, foodborne, bovine tuberculosis or losing your mind for the sake of a shake or burger. Broxmeyer L et al; Med Hypotheses. 2005;64(4):699-705; & (d) Association between dietary patterns and cognitive function among 70-year-old Japanese elderly: a cross-sectional analysis of the SONIC study. Okubo H et al; Nutr J. 2017 Sep 11;16(1):56; & (e) Relationships of Dietary Patterns, Foods, and Micro- and Macronutrients with Alzheimer's Disease and Late-Life Cognitive Disorders: A Systematic Review. Solfrizzi V et al;
J Alzheimers Dis.
 2017;59(3):815-849; & (f) Chronic Neurodegenerative Illnesses and Epilepsy in Danish Adventists and Baptists: A Nationwide Cohort Study. Thygesen et al.  J Alzheimers Dis.  2017;56(4):1429-1435.


(110) (a) Quig D, Doctors Data Lab,"Cysteine  metabolism and metal  toxicity", Altern Med Rev,       1998;3:4, p262‑270, & (b)  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;   

(111) Hyperhomocysteinemia: a new risk factor for degenerative diseases. Herrmann W et al; Clin Lab. 2002;48(9-10):471-81; & (b) Effects of dietary supplementation with creatine on homocysteinemia and systemic microvascular endothelial function in individuals adhering to vegan diets. Van Bavel D et al; Fundam Clin Pharmacol. 2018 Dec 3.

(112) Copper-2 Ingestion, Plus Increased Meat Eating Leading to Increased Copper Absorption, Are Major Factors Behind the Current Epidemic of Alzheimer's Disease. Brewer GJ; Nutrients. 2015 Dec 2;7(12):10053-64; & (b) Copper-2 Hypothesis for Causation of the Current Alzheimer's               ok[pokl i9Disease Epidemic Together with Dietary Changes That Enhance the Epidemic. Brewer G J et al; Chem Res Toxicol. 2017 Mar 20;30(3):763-768.

(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) (a) Metal Toxicity Links to Alzheimer's Disease and Neuroinflammation. J Mol Biol. 2019 Jan 18. Huat TJ et al; & (b) Biometal Dyshomeostasis and Toxic Metal Accumulations in the Development of Alzheimer's Disease. Front Mol Neurosci. 2017 Oct 24;10:339. Li Y, JiangH, et al; & Identifying key genes, pathways and screening therapeutic agents for manganese-induced Alzheimer disease using bioinformatics analysis. Medicine (Baltimore). 2018 Jun;97(22), Ling J et al; & Thematic Review Series: ApoE and Lipid Homeostasis in Alzheimer’s Disease: Cellular cholesterol homeostasis and Alzheimer’s disease; Ta-Yyan Chang et al; J Lipid Res. 2017 Dec; 58(12): 2239–2254. 


(115) 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. 

(116) Tofu intake is associated with poor cognitive performance among community-dwelling elderly in China. Xu X et al; J Alzheimers Dis. 2015;43(2):669-75; & (b) Nutrition research in cognitive impairment/dementia, with a focus on soya and folate. Hogervorst E et al; Proc Nutr Soc. 2017 Nov;76(4):437-442

(119) (a)  L.Ronnback et al, "Chronic encephalopaties induced by low doses of mercury or lead",   Br J Ind Med 49: 233-240, 1992; &(b) H.Langauer‑Lewowicka,” Changes in the nervous system due to occupational metallic mercury poisoning” Neurol Neurochir Pol 1997 Sep‑Oct;31(5):905‑13; & Langauer-Lewowicka H.  [Chronic toxic encephalopathies]    [Polish]   Med Pr. 1982;33(1-3):113-7.

(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;& 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.  & 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 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.


(158) The relationship of the toxic effects of mercury to exacerbation of the medical condition classified as Alzheimer’s disease, B.E. Haley, Medical Veritas 4 (2007) 1510–1524, & (b) F.L.Lorscheider,B.Haley,et al, “Mercury vapor inhibits tubulin   binding...”, FASEB J,9(4):A-3485.,1995 &(c) Wenstrup et al, “Trace element imbalances in the brains of Alzheimers patients”, Research, Vol 533,p125-131,1990;& (d) Vance et al, 1988, Neurotoxicology, 9:197-208; &  (e) de Saint-Georges et al, “Inhibition by mercuric chloride of the in vitro polymeriztion of microtubules”, CR Seances Soc Biol Fil, 1984; 178(5):562-6

(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’s disease”,  1989, 8(3):128-41.

(174) B.Willershausen et al, “Mercury in the mouth mucosa of patients with amalgam fillings”, Dtsch Med Wochenschr, 1992, 117:46, 1743-7

(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.

(192) N.Nogi, “Electric current around dental metals as a factor producing allergic metal ions in the oral cavity”, Nippon Hifuka Gakkai Zasshi, 1989, 99(12):1243-54;  & J. Bergdahl,  A.J.Certosimo et al, National Naval Dental Center, “Oral Electricity”, Gen Dent, 1996, 44(4):324-6; &    R.H.Ogletree et al, School of Materials Science, GIT, Atlanta,”Effect of mercury on corrosion of eta’ Cu-Sn phase in dental amalgams”, Dent Mater, 1995, 11(5):332-6;   & R.D.Meyer et al, “Intraoral galvanic corrosion”,Prosthet Dent, 1993,69(2):141-3; & B.M.Owens et al, “Localized galvanic shock after insertion of an amalgam restoration”, Compenium, 1993, 14(10),1302,1304,1306-7; & Johansson E, Liliefors T, "Heavy elements in root tips from teeth with amalgam fillings", Department of Radiation Sciences, Division of Physical Biology, Box 535, 751 21 Uppsala, Sweden

(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 deficiency”, Ann Neural, 1985, 18(4):482-489.

(198) Cd2+ and Hg2+ affect glucose release and cAMP-dependent transduction pathway in isolated eel hepatocytes. Aquat Toxicol. 2003 Jan 10;62(1):55-65, Fabbri E, Caselli F, Piano A, Sartor G, Capuzzo A. &  Fluctuation of trace elements during methylmercury toxication and chelation therapy. Hum Exp Toxicol. 1994 Dec;13(12):815-23, Bapu C, Purohit RC, Sood PP; &   E.S. West et al, Textbook of Biochemistry, MacMillan Co, 1957,p853;&  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, Neurotoxicol. Teratol.,  18:129-134;

(199) Dr. P.Kraub & M.Deyhle, Universitat Tubingen- Institut fur Organische Chemie, “Field  Study on the Mercury Content of Saliva”, 1997   http://www.uni‑;  

(20,000 people tested for mercury level in saliva and health status/symptoms compiled)

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

(207) Pendergrass JC, Haley BE, Univ. Of Kentucky Dept. Of Chemistry “ The Toxic Effects of 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 1997, 18(2)::315-24;   &  Met Ions Biol Syst, 1997, 34:461-, & Palkiewicz P, Zwiers H, Lorscheider FL;    ADP‑Ribosylation of Brain Neuronal Proteins Is Altered by In Vitro and In Vivo Exposure to Inorganic Mercury,  Journal of Neurochemistry. 62(5):2049‑2052, 1994 May

(217) Agency for Toxic Substances and Disease Registry, U.S. Public Health   Service, Toxicological Profile for          Mercury , 1999; & Apr 19,1999 Media Advisory, New MRLs for toxic substances, MRL:elemental mercury vapor/inhalation/chronic & MRL:   methy mercury/ oral/acute; &

(221) R. Golden et al, Duke Univ., “Dementia and Alzheimer’s Disease”, Minnesota Medicine, 78:p25-29, 1995; & Schofield P, Dementia associated with toxic causes and autoimmune disease.  Int Psychogeriatr. 2005;17 Suppl 1:S129-47.
(232)Adolph Coors Foundation, “Coors Amalgam Study: Effects of placement and removal of amalgam fillings”, 1995. (www) & Internations DAMS 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. ( (over 1000 cases)   (Sweden has banned amalgam fillings & Gov’t maintains health records on all citizens) ; & Heavy Metal Bulletin, No.3,1996 and No.1, 1999, p7,8; &  Klock B, Blomgren J, Ripa U, Andrup B, "Effekt av amalgamavlägsnande på patienter som misstänker att de lider eller har lidit av amalgamförgiftning", Tandläkartidn 81(23):1297-1302 (1989)       .

(234) P.E. Bigazzi, “Autoimmunity and Heavy Metals”, Lupus, 1994; 3: 449-453; & Pollard KM, Pearson Dl, Hultman P.  Lupus-prone mice as model to study xenobiotic-induced autoimmunity.  Envriron Health Perspect 1999; 107(Suppl 5): 729-735; & Nielsen JB; Hultman P.  Experimental studies on genetically determined susceptibility to mercury‑induced autoimmune response.   Ren Fail 1999 May‑Jul;21(3‑4):343‑8; & Hultman P, Enestrom S, Mercury induced antinuclear antibodies in mice,  Clinical and Exper Immunology, 1988, 71(2): 269-274.

(242) J.Constantinidis et al, Univ. Of Geneva Medical School, “Hypothesis   regarding amyloid and zinc in the pathogenisis of Alzheiemer Disease”,   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’s disease”,  J Neural Transm Park Dis Dement Sect 1991; 3(4):231-

(257)  I. Smith et al, “Pteridines and   mono-amines: relevance to neurological damage”, Postgrad Med J, 62(724): 113-123, 1986; &  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”, Science, 219(4580):75-77, Jan 1983; & T.Nagatsu et al, “Catecholoamine-related enzymes and the biopterin cofactor in Parkinson’s”, Neurol, 1984, 40: 467-73.

(258) Ely, J.T.A., Mercury Induced Alzheimer’s Disease: Accelerating Incicdence?, Bull Environ Contam Toxicol,  2001, 67: 800-6.

(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 Porphyrinogenic Metals 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)    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; & Kurup RK, Kurup PA.   Hypothalamic digoxin, hemispheric chemical dominance, and Alzheimer's disease.   Int J Neurosci. 2003 Mar;113(3):361-81.

(275) American Journal of Human Genetics,, Aug 2008  

(276)  ATSDR/EPA Priority List for 2005: Top 20 Hazardous Substances, Agency for Toxic Substances and Disease Registry, U.S. Department of Health and Human Services,

(280) S.Nonaka et al, Nat. Inst. of Mental Health, Bethesda Md., “Lithium treatment  protects neurons in CNS from glutamate induced  excitibility and calcium influx”,  Neurobiology, Vol 95(5):2642-2647, Mar 3, 1998; & 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; & Chuang D. Et al, National Institute of Mental Health, Science News, Nov 11, 2000, 158:309; & Science News, 3-14-98,   p164;   & Moore al, Lancet Oct 7, 2000; & Science News, 10-31-98, p276; & (b) 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.

(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):F830-6.   & Anner BM, Moosmayer M.  Mercury inhibits Na-K-ATPase primarily at the cytoplasmic side.  Am J Physiol 1992; 262(5 Pt2):F84308; & 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):F926-30;  &   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 [3H]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.

(289) J.Mai et al, Biological Trace Element Research,1990;24:109-117 (antioxidants reduce effects of MS)


(291) H.A. Huggins,  Solving the MS Mystery, 2002,  & ; & H.A.Huggins & TE Levy, “cerebrospinal fluid protein changes in MS  after  Dental amalgam  removal”,   Alternative Med Rev, Aug 1998, 3(4):295-300.

(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. 

(300) C.Hock et al, “Increased blood mercury levels in patients with Alzheimer’s disease”, J. Neural Transm, 1998, 105(1):59-68.

(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 Parkinson’s”,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 Alzheimer’s's 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 erythrmatosus(SLE)”, Lancet, 1992, 339:8784,            25-6; & P.Emory et al, “Poor sulphoxidation in patients with rheumatoid arthitis”, Ann Rheum  Dis, 1992,                51:3,318-20; & 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,           “Hallevorden-Spatz Disease: cysteine accumulation and cysteine dioxygenase defieciency”, Ann Neural, 1985,             18(4):482-489.

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

(335) A. Engqvist et al, “Speciation of mercury excreted in feces from individuals with amalgam fillings”,         Arch Environ Health, 1998, 53(3):205-13; & Dept. of Toxicology & Chemistry, Stockholm Univ.,                National Institute  for Working Life, 1998 (

(338) (a)W.Y.Boadi et al, Dept. Of Food Engineering and Biotechnology, T-I Inst of Tech., Haifa, Israel, “In vitro        effect of mercury on enzyme activities and its accumulation in the first-trimester human placenta”, Environ             Res, 1992, 57(1):96-106;&       “In vitro exposure to mercury and cadmium alters term human placental            membrane fluidity”, Pharmacol, 1992, 116(1): 17-23;  & (b)J.Urbach et al, Dept. of Obstetrics & Gynecology,              Rambam Medical Center, Haifa, Israel, “Effect of inorganic mercury on in vitro      placental nutrient transfer        and oxygen consumption”, Reprod Toxicol, 1992,6(1):69-75;& ©  Karp W, Gale TF et al, Effect of mercuric            acetate on selected        enzymes of maternal and fetal hamsters” Environmental Research, 36:351-358; &  W.B.           Karp et al, “Correlation of human placental enzymatic  activity with tracemetal concentration in placenta”,           Environ   Res. 13:470-477,1977; & (d)  Boot JH.  Effects of SH‑blocking compounds on the energy metabolism         and glucose uptake in isolated rat  hepatocytes.  Cell Struct Funct 1995 Jun;20(3):233‑8; &(e) H.Iioka et al, “The effect of inorganic mercury on placental amino acid transport”, Nippon sanka Fujinka Gakkai Zasshi, 1987, 39(2): 202-6.

(346) Clauw DJ, “The pathogenesis of chronic pain and fatigue syndroms: fibromyalgia” Med Hypothesis,     1995,  44:369-78; & Hanson S,  Fibromyalgia, glutamate, and mercury.   Heavy Metal Bulletin, Issue 4,     1999, 

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

(372) Atchison WD.  Effects of neurotoxicants on synaptic transmission. Neuroltoxicol Teratol 1998,               10(5):393-416;  &   Sidransky H, Verney E, Influence of lead acetate and selected metal salts on                tryptophan binding to rat  hepatic nuclei.  Toxicol Pathol 1999, 27(4):441-7; & Shukla GS, Chandra SV, Effect of interaction of Mn2+withZn2+, Hg2+, and Cd2+ on some neurochemicals in rats. Toxicol Lett 1982, 10(2-3):163-8; & Brouwer M et al, Functional changes induced by heavy   metal ions.    Biochemistry, 1982, 21(20): 2529-38.

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

(416) ( c) 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;  

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

(425) (a) Hu H; Abedi‑Valugerdi M; Moller G.   Pretreatment of lymphocytes with mercury in vitro induces  a response in T cells from genetically determined low‑responders and a shift of the interleukin profile.  Immunology 1997 Feb;90(2):198‑204; & (b) Hu H; Moller G; Abedi‑Valugerdi M.  Major histocompatibility complex class II antigens are required for both cytokine production and proliferation induced by mercuric chloride in   vitro.  J Autoimmun 1997 Oct;10(5):441‑6; & (c) Hu H; Moller G; Abedi‑Valugerdi M.  Mechanism of mercury‑induced autoimmunity: both T helper 1‑ and T helper 2‑type responses are involved.  Immunology 1999      Mar;96(3):348‑57; & (d) HultmanP, Johansson U, Turley SJ; Adverse immunological effects and autoimmunity induced by dental amalgam in mice.  FASEB J 1994; 8: 1183-90; &(e) Pollard KM, Lee DK, Casiano CA; The autoimmunity-inducing xenobiotic mercury interacts with the autoantigen fibrillarin and modifies its molecular structure and antigenic properties.  J Immunol 1997; 158: 3421-8; & (f) Abedi-Valugerdi M, Hansson M, Moller G., "Genetic control of resistance to mercury-induced immune/autoimmune activation", Scand J Immunol, 54(1-2):190-7 (Jul-Aug 2001) 

(426) Hultman P, Nielsen JB.  The effect of toxicokinetics on murine mercury-induced autoimmunity. Environ Res 1998, 77(2): 141-8; & Hultman et al, "Activation of the immune system and systemic immune-complex deposits in Brown Norway rats with dental amalgam restorations", J Dent Res, 77(6):1415-25, (Jun 1998)

(430) Fukino H, Hirai M, Hsueh YM, Yamane Y.  Effect of zinc pretreatment on mercuric chloride-induced lipid         peroxidation in the rat kidney.  Toxicol Appl Pharmacol 1984, 73(3): 395-401.

(432) Sutton KG, McRory JE, Guthrie H, Snutch TP.   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):575-9

(435) Does Inorganic Mercury Play a Role in Alzheimer’s Disease? A Systematic Review and an Integrated Molecular Mechanism; Joachim Mutter, Annika Curth, Johannes Naumann, Richard Deth, and Harald Walach, Journal of Alzheimer’s Disease, 2010; &(b) [Mercury and Alzheimer's disease]. Mutter J, Walach H, et al; Fortschr Neurol Psychiatr. 2007 Sep;75(9):528-538.


(436) Schiwara, H.-W.  (Medical Laboratory) Arzte fur Laboratoriumsmedizen, D-28357 Bremen; & Heavy Metal Bul, 1999, 1:28.

(437) Mercury Toxicity and Alzheimer’s Disease, Cognitive Enhancement Research Institute & (b)   Amer. College of Medical Genetics Working Group on ApoE and Alzheimer’s, JAMA, 1995,274:1627-29; &   Godfrey ME, Wojcik DP, Krone CA.  Apolipoprotein E genotyping as a potential biomarker for mercury neurotoxicity. J Alzheimers Dis. 2003 Jun;5(3):189-95, & © Joachim Mutter, Harald Walach et al; Alzheimer Disease: Mercury as pathogenetic factor and apolipoprotein E as a moderator, Neuroendocrinology Letters No.5 October Vol.25, 2004

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

(444) (a) Beal MF. Coenzyme Q10 administration and its potential for treatment of neurodegenerative diseases. Biofactors 1999, 9(2-4):262-6; & 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, Baik M, 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.  Neurosci Lett 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; & (d) Kidd PM., Neurodegeneration from mitochondrial insufficiency: nutrients, stem cells, growth factors,  and prospects for brain rebuilding using integrative management. Altern Med Rev. 2005 Dec;10(4):268-293.

(445) Inflammation, depression and dementia: are they connected?  Neurochem Res. 2007 Oct;32(10):1749-56. Epub 2007 Aug 20  Leonard BE; & Vaccines, Depression and Neurodegeneration After Age 50, By Russell L. Blaylock,

(450) Dr. S J Walsh and L M Rau,  University of Connecticut Health Center,     “Autoimmune Disease Overlooked as a Leading Cause of Death in Women.   Am J Public Health 2000;90:1463‑1466.

(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. 

(464)  Walsh, WJ, Health Research Institute, Autism and Metal Metabolism,, Oct        20, 2000; &             Walsh WJ, Pfeiffer Treatment Center, Metal‑Metabolism and Human Functioning,   2000,;

(469), the book, by  David Perlmutter MD;  Perlmutter Health Center, Naples, Florida,          

(470) V Rondeau, D Commenges, H Jacqmin‑Gadda and JF Dartigues,  . Relation between aluminum      concentrations in drinking water and Alzheimer's disease: an 8‑year follow‑up study.  American Journal of Epidemiology, Vol 152, Issue 1 59‑66; & (b)Aluminium in Alzheimer's disease: are we still at a crossroad? Gupta VB, Anitha S, Jagannatha Rao KS.  Cell Mol Life Sci. 2005 Jan;62(2):143-58

(475)  Hugh Fudenberg, MD,  paper: NVIC International Vaccine Conference, Arlington, VA                        September, 1997.     (

(477) Lars Landner and Lennart Lindestrom.   Swedish Environmental Research Group(MFG), Copper in society                 and the Environment, 2nd revised edition. 1999.

(485) Hulda Clark, The Cure for all Diseases, 2000,  (amalgam replacement, dental revision, detoxification, and treatment for parasites)  

(488)    Huang X; Cuajungco MP et al;   Cu(II) potentiation of alzheimer abeta neurotoxicity. Correlation with cell‑free        hydrogen peroxide  production and metal reduction.  J Biol Chem 1999 Dec 24;274(52):37111‑6


(489)  Waggoner DJ, Bartnikas TB, Gitlin JD.  The role of copper in neurodegenerative disease.  Neurobiol Dis 1999 Aug;6(4):221‑30; & (b) Torsdottir G et al; Copper, ceruloplasmin and superoxide dismustase) in amyotrophic lateral sclerosis. Pharmacol Toxicol 2000 Sep;87(3):126‑30; & © Estevez AG,Beckman JS et al,   Induction of nitric oxide‑dependent apoptosis in motor neurons by  zinc‑deficient superoxide dismustase.  Science 1999 Dec 24;286(5449):2498‑500; &(d) Cookson MR, Shaw PJ.   Oxidative stress and motor neurons disease. Brain Pathol 1999 Jan;9(1):165‑86.

(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; & 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; & 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); & (b)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); & © “Decreased phagocytosis of myelin by macrophages with ALA.   Journal of   Neuroimmunology 1998, 92:67-75; & (d) & Z. Gregus et al, “Effect of lipoic acid on biliary excretion of glutathione and metals”, Toxicol APPl Pharmacol, 1992, 114(1):88-96; & (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

(495) Kang JH, Eum WS.  Enhanced oxidative damage by the familial amyotrophic lateral sclerosis‑associated     Cu,Zn‑superoxide dismustase mutants.  Biochem Biophys Acta 2000 Dec 15;1524(2‑3):162‑70; & (b) JH, Eum WS.  Enhanced oxidative damage by the familial amyotrophic lateral sclerosis‑ associated Cu,Zn‑superoxide     dismustase mutants.  Biochem Biophys Acta 2000 Dec 15; 1524(2‑3): 162‑70; & ©    Liu H, Zhu H, Eggers DK, Nersissian AM, Faull KF, Goto JJ, Ai J, Sanders‑Loehr J,  Gralla EB, Valentine JS.   Copper(2+) binding to the surface residue cysteine 111 of His46Arg  human copper‑zinc superoxide dismustase, a familial amyotrophic   lateral sclerosis mutant.  Biochemistry 2000 Jul 18;39(28):8125‑32; &(d) Wong PC, Gitlin JD; et al, Copper chaperone for superoxide dismustase is essential to activate   mammalian Cu/Zn superoxide dismustase.   Proc Natl Acad Sci U S A 2000 Mar 14;97(6):2886‑91; & (e)Kruman II, Pedersen WA, Springer JE, Mattson MP.   ALS‑linked Cu/Zn‑SOD mutation increases vulnerability of motor  neurons to excitotoxicity by a mechanism involving increased oxidative stress and perturbed calcium homeostasis.  Exp Neurol 1999 Nov;160(1):28‑39

(496)  Doble A. The role of excitotoxicity in neurodegenerative disease: implications   for therapy.  Pharmacol Ther       1999 Mar;81(3):163‑221; &      Urushitani M, Shimohama S.  N‑methyl‑D‑aspartate receptor‑mediated   mitochondrial Ca(2+)  overload in acute excitotoxic motor neuron death: a mechanism  distinct from chronic   neurotoxicity after Ca(2+) influx.   J Neurosci Res 2001 Mar 1;63(5):377‑87; &   Cookson MR, Shaw PJ.           Oxidative stress and motor neurons disease.  Brain Pathol 1999 Jan;9(1):165‑86

(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 ) Shukla PK, Khanna VK, Khan MY, Srimal RC. Protective effect of curcumin against lead neurotoxicity in rat. Hum Exp Toxicol 2003;22:653-8. 

(498) Daniel S, Limson JL, Dairam A, Watkins GM, Daya S. 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

(502) (a)Dr. Gerald Bernstein, Beth Israel Medical Center, NY, past Pres., Amer. Diabetes Association; &              .         U.S. Centers for Disease Control, 2001,; 

         & Anthony Iacopino.Conference Paper,American Academy of Periodontology(AAP)at 

     the US National Institutes of Health in Bethesda, Maryland, April, 2001; & (b)Diabetes: A Silent Epidemic, Newsweek, Sep 4, 2000  Harris Coulter, Childhood Vaccinations and Juvenile‑Onset (Type‑1) Diabetes,   Testimony before the Congress of the United States, House of Representatives, Committee on Appropriations, subcommittee on Labor, Health and Human Services, Education, and Related Agencies,  April 16, 1997, ; & (c) Dr. Bart Classen, Vaccines are the largest cause of insulin-dependent diabetes in young children,  paper given at American College for Advancement in Medicine., Nashville, Tenn., May 14, 2001; &   Classen B. ,Autoimmunity August 2002 Vol. 35 (4), pp. 247-253 & Swedish researchers, Ann. N.Y. Acad Sci. 958: 293-296, 2002, &

(d) Narayan KMV, Boyle JP,Lifetime risk for diabetes mellitus in the U.S.   JAMA, 2003, 290(14):1884-90; &  (e) W. Block, Lipoic Acid Helps Fight Diabetes, Life Enhancement, Dec 2003;                        

(503) Protective effects of methylcobalamin, a vitamin B12 analog, against glutamate- induced neurotoxicity in retinal cell culture.  Kikuchi M, Kashii S, Honda Y, Tamura Y, Kaneda K, Akaike A.  Invest Ophthalmol Vis Sci. 1997 Apr;38(5):848-54;  van Rensburg SJ, Kotze MJ, Hon D, Haug P, Kuyler J, Hendricks M, Botha J, Potocnik FC, Matsha T, Erasmus RT.   Metab Brain Dis. 2006 Sep;21(2-3):121-37. Epub 2006 May 26; & van Rensburg SJ, Kotze MJ, Hon D, Haug P, Kuyler J, Hendricks M, Botha J, Potocnik FC, Matsha T, Erasmus RT.   Metab Brain Dis. 2006 Sep;21(2-3):121-37. Epub 2006 May 26

(504) Activation of methionine synthase by insulin-like growth factor-1 and dopamine: a target for neurodevelopmental toxins and thimerosal,  Waly M, Olteanu H, Deth RC et al, Mol Psychiatry. 2004 Apr;9(4):358-70; & Mercury and multiple sclerosis, Clausen J.   Acta Neurol Scand. 1993 Jun;87(6):461-4

(505) Chemical methylation of inorganic mercury with methylcobalamin, a vitamin B12 analog.  Imura N,  Pan SK,  Ukita T et al.  Science. 1971 Jun 18; 172(989): 1248-9; & Cobalamin-mediated mercury methylation by Desulfovibrio desulfuricans LS, Choi SC, Bartha R.    Appl Environ Microbiol. 1993 Jan;59(1):290-5, & Isolation of the provisionally named Desulfovibrio fairfieldensisfrom human periodontal pockets,  Loubinoux J.; Bisson-Boutelliez C.; Miller N.; Le Faou A.E. Oral Microbiology and Immunology, Volume 17, Number 5, October 2002 , pp. 321-323(3)

(507) Appel SH, Beers D, Siklos L, Engelhardt JI, Mosier DR.  Calcium: the Darth Vader of ALS. Amyotroph Lateral  SclerOther Motor Neuron Disord 2001 Mar;2 Suppl 1:S47-54; 

(517) Earl C, Chantry A, Mohammad N.   Zinc ions stabilize the association of basic protein with brain myelin        membranes.  J Neurochem 1988; 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: Chang L(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. 

(521) Guermonprez L, Ducrocq C, Gaudry-Talarmain YM.  Inhibition of acetylcholine synthesis and tyrosine         nitration induced by peroxynitrite are differentially prevented by antioxidants.  Mol Pharmacol 2001        Oct;60(4):838-46; & 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.

(524) Urushitani M, Shimohama S.  The role of nitric oxide in amyotrophic lateral sclerosis. Amyotroph Lateral Scler Other Motor Neuron Disord 2001 Jun;2(2):71-81; & Torreilles F, Salman-Tabcheh S, Guerin M, Torreilles J. Neurodegenerative disorders: the role of peroxynitrite.Brain Res Brain Res Rev 1999 Aug;30(2):153-63; & Aoyama K, Matsubara K, Kobayashi S.  Nitration of manganese superoxide dismutase in cerebrospinal fluids is a marker for peroxynitrite-mediated oxidative stress in neurodegenerative diseases.   Ann Neurol 2000 Apr;47(4):524-7; & Guermonprez L, Ducrocq C, Gaudry-Talarmain YM.  Inhibition of acetylcholine synthesis and tyrosine nitration induced by peroxynitrite aredifferentially prevented by antioxidants.  Mol Pharmacol 2001 Oct;60(4):838-46


(543)  U.S. Centers for Disease Control, National Center for Health Statistics,  NHANES III 

study(thousands of people’s health monitored), ;  &  ; & 

(b) Laks, Dan R. Assessment of chronic mercury exposure within the U.S. population, 

National Health and Nutrition Examination Survey, 1999–2006. Biometals. August 2009; & 

Laks, D.R. et al, Mercury has an affinity for pituitary hormones, Medical Hypotheses, Dec 

2009; & (c) An Investigation of Factors Related to Levels of Mercury in Human Hair,   

Environmental Quality Institute, October 01, 2005,


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

(577) Mutter J, Daschner F, et al, Amalgam risk assessment with coverage of references up to 2005] ,   Gesundheitswesen. 2005 Mar;67(3):204-16.  &

(580) Life Extension Foundation (MDs), Disease Prevention and Treatment, Expanded 4th Edition, 2003 ,

(581) Brain Health and Blood Sugar,  Vitamin Research News, Vol 23, No.1, Jan 2009, p1-5. 

(582) Insulin resistance-associated hepatic iron overload. Gastroenterology. 1999 Nov;117(5):1155-63, Mendler MH, Turlin B, Moirand R, et al. 

(585) Aluminum Hydroxide: Another Poison Pediatricians Inject in Babies; IMVA, ; & (b) “Vaccines Show Sinister Side” March 23,2006, ; (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)

(586)  Repeated Exposure to Pesticides Increases Alzheimer's Disease Risk, K. M. Hayden , Neurology. 2010;74:1524-1530

(589) Association between dental amalgam fillings and Alzheimer's disease: a population-based cross-sectional study in Taiwan.  Sun YH, Alzheimers Res Ther. 2015 Nov 12;7(1):65; &  (b) Mercury Involvement in Neuronal Damage and in Neurodegenerative Diseases. Cariccio VL et al; Biol Trace Elem Res. 2019 Feb;187(2):341-356. & (d) Associations of blood mercury, inorganic mercury, methyl mercury and bisphenol A with dental surface restorations in the U.S. population, NHANES 2003–2004 and 2010–2012. Lei Yin et al; Ecotoxicology and Environmental Safety, 2016; 134: 213 

(590) (a)Current status of metals as therapeutic targets in Alzheimer's disease, Finefrock AE etal, J Am Geriatr Soc. 2003 Aug;51(8):1143-8; & (b)Metals in our minds: therapeutic implications for neurodegenerative disorders,  Doraiswamy PM, Finefrock AE., Lancet Neurol. 2004 Jul;3(7):431-4 & (c)Perry G et al, . The role of iron and copper in the aetiology of neurodegenerative disorders.CNS Drugs 2002;16:339-52; &(d) DAI, Xueling; SUN, Yaxuan; JIANG. Zhaofeng Copper (2) potentiation of Alzheimers A-(beta)1-40 cytotoxicity and transition on its secondary structure. Acta Biochimica et Biophysica Sinica 1938;11:765-72.; & (e)Liu G et al. Metal exposure and Alzheimers pathogenesis. J Structural Biol 2005;155:45-51.  

 (591) The interaction of melatonin and its precursors with aluminium, 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) Should Depressive Syndromes Be Reclassified as "Metabolic Syndrome Type II"?  Ann Clin Psychiatry. 2007 Oct-Dec;19(4):257-64. McIntyre RS, Soczynska JK, Kennedy SH et al;& Inflammation, depression and dementia: are they connected?  Neurochem Res. 2007 Oct;32(10):1749-56. Epub 2007 Aug 20  Leonard BE.

(593) Vaccines, Depression and Neurodegeneration After Age 50, By Russell L. Blaylock,; &(b) Immunoexcitotoxicity, R L Blaylock, Alt Ther Health Med, 2008, 14:46-53; & (c) Beat Depression and Anxiety with Diet/Nutrition, Blaylock Report, Dec 2010.  

(594) Heavy Metal and Chemical Toxicity,  Dietrich Klinghardt, MD, Ph.D. ; & 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  

(595) High fructose consumption combined with low dietary magnesium intake may increase the incidence of the metabolic syndrome by inducing inflammation. Magnes Res. 2006 Dec;19(4):237-43. Rayssiguier Y, Gueux E, et al; & (b) Dietary magnesium and fiber intakes and inflammatory and metabolic indicators in middle-aged subjects from a population-based cohort. Am J Clin Nutr. 2006 Nov;84(5):1062-9 Bo S, Durazzo M, Pagano G. et al; & (c) Hypomagnesemia, oxidative stress, inflammation, and metabolic syndrome.  Diabetes Metab Res Rev. 2006 Nov-Dec;22(6):471-6. Guerrero-Romero F, Rodríguez-Morán 

(596) Effects of antidiabetic and antihyperlipidemic agents on C-reactive protein.  Mayo Clin Proc. 2008 Mar;83(3):333-42, Dandona P; & Role of advanced glycation end products in hypertension and atherosclerosis: therapeutic implications. Cell Biochem Biophys. 2007;49(1):48-63, Vasdev S, Gill V, Singal P.

(597) Effects of mercuric chloride on glucose transport in 3T3-L1 adipocytes.  Toxicol In Vitro. 2005 Mar;19(2):207-14.  Barnes DM, Kircher EA; & Effects of inorganic HgCl2 on adipogenesis. Toxicol Sci. 2003 Oct;75(2):368-77. Epub 2003 Jul 25, Barnes DM, Hanlon PR, Kircher EA; & (b) Heavy metal-induced inhibition of active transport in the rat small intestine in vitro. Interaction with other ions. Comp Biochem Physiol C. 1986;84(2):363-8, Iturri SJ, Peña A; & Interaction of the sugar carrier of intestinal brush-border membranes with HgCl2. Biochim Biophys Acta. 1980 May 8;598(1):100-14, Klip A, Grinstein S, Biber J, Semenza G.

(598) Overcoming Depression,  Dr. Russell Blaylock, The Blaylock Wellness Report, Vol 5, No. 3, March 2008; & The Blaylock Wellness Report, Inflammatory Conditions, Vol 5, No. 3, Feb 2008, & Food Additives, What you eat can kill you, Vol 4, No. 10,

(599) High fructose consumption combined with low dietary magnesium intake may increase the incidence of the metabolic syndrome by inducing inflammation. Magnes Res. 2006 Dec;19(4):237-43. Rayssiguier Y, Gueux E, et al; & (b) Dietary magnesium and fiber intakes and inflammatory and metabolic indicators in middle-aged subjects from a population-based cohort. Am J Clin Nutr. 2006 Nov;84(5):1062-9 Bo S, Durazzo M, Pagano G. et al; & (c) Hypomagnesemia, oxidative stress, inflammation, and metabolic syndrome.  Diabetes Metab Res Rev. 2006 Nov-Dec;22(6):471-6. Guerrero-Romero F, Rodríguez-Morán 


 (600) Annotated bibliography: Exposure levels and health effects related to mercury/dental amalgam and results of amalgam replacement ;B Windham(Ed.),(over 3000 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)              

(601) Cognitive and Behavioral Effects of Toxic Metal Exposures; B. Windham (Ed), (over 150 medical study references

(602) The mechanisms by which mercury causes chronic immune and inflamatory condtions,B.Windham(Ed.),

(603) The environmental effects of mercury from amalgam affect everyone. B. Windham (Ed.)  (Gov’t studies)

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

(605) Mechanisms of mercury release from amalgam dental fillings: vaporization, oral galvanism, and effects of Electromagnetic fields,       

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

(607) Documentation of mercury exposure levels from dental amalgam,


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 doesnt think them necessary here.