Mercury Contributes To Alzheimer's Disease!

"You wouldn’t take a leaky thermometer, 

put it in your mouth, and leave it there 24 hours a day, 

365 days a year. Yet that’s exactly what happens 

when an amalgam filling is installed in your mouth."

Dr Michael Ziff

Link between Mercury and Alzheimer’s Disease

Research conducted at the University of Calgary Faculty of Medicine has demonstrated that trace amounts of mercury can cause the type of damage to nerves that is characteristic of the damage found in Alzheimer’s Disease. The level of mercury exposure is consistent with those levels found in humans with mercury/silver amalgam dental fillings. The exposure to mercury caused the formation of “neurofibrillar tangles,” which are one of the two diagnostic markers for Alzheimer’s Disease.

The scientists found that other metals, including aluminum, did not cause the damage. Previous research has shown that mercury can cause the formation of the other Alzheimer’s Disease diagnostic marker, “amyloid plaques.”

This study should remove all doubt regarding the role that dental mercury from amalgam fillings plays in the development of Alzheimer’s Disease (AD). Although the American Dental Association would like to have you believe otherwise, science has clearly demonstrated that there is a positive correlation between brain mercury levels and the number and surfaces of “mercury/silver” amalgam dental fillings. The mercury levels that caused the devastating damage to nerve cells in the above referenced study were 100 to 1000 times below those found in the brains of people with “mercury/silver” amalgam dental fillings.

In 1997, researchers at the University of Calgary Medical School and the College of

Pharmacy at the University of Kentucky clearly demonstrated that exposing rats to the same levels of mercury vapor that can be released from “mercury/silver” amalgam dental fillings caused the mercury to interact with brain tubulin and disassemble microtubles that maintain neurite structure. The identical neurochemical lesion of similar or greater magnitude is evident in Alzheimer brain homogenates from approximately 80% of patients, when compared to human age-matched neurological controls.

In 2000, researchers at the Neurobiology Laboratory, Psychiatric University Hospital in Basel, Switzerland using neuroblastoma cells exposed to mercury demonstrated an increase in production of amyloid protein that makes up the amyloid plaques as well as significantly increasing the phophorylation of Tau protein.

Mercury Sources

Major human sources of mercury in the human bodies include fish consumption, dental amalgams and vaccines. Methyl mercury in fish, being bound to cysteine, appears to be by far less toxic than hitherto assumed and is about 20 times less toxic than methyl mercury chloride. For that reasons, methyl-mercury found in fish seems not to be involved in the pathogenesis of Alzheimer’s disease. Inorganic mercury (found in dental amalgam) or ethyl-mercury (found in vaccines) may play a major role.

Dental amalgam, the silver fillings dentists use, is by far the biggest culprit of mercury poisoning and the biggest reason for Alzheimer's and dementia in the world today.

According to Hugh Fudenberg, MD, the world's leading immunogeneticist and 13th most quoted biologist of our times (nearly 850 papers in peer review journals): “If an individual has had 5 consecutive flu shots between 1970 and 1980 (the years studied) his/her chances of getting Alzheimer's Disease is 10 times higher than if he/she had one, 2 or no shots”. Dr. Fudenberg said it was so and that it was due to mercury and aluminum that is in every flu shot. The gradual mercury and aluminum buildup in the brain causes cognitive dysfunction. Flu shots contain 25 micrograms of mercury. One microgram is considered toxic.

"The maximum amount of mercury that the Environment Protection Agency allows people to be exposed to is 5,000 times smaller than the permissible amount of lead exposure; in other words the EPA apparently considers mercury to be 5,000 times more toxic than lead."
Marcia Basciano DDS at annual meeting of IAOMT San Diego 1994

Estimates of amounts of mercury absorbed from amalgams

That amalgams can double the body's mercury level and triple the urine's mercury level suggests that mercury from amalgams is the source of at least half to two-thirds of all the mercury humans are exposed to. Over the last four or five years, a substantial body of evidence has emerged which indicates that most of the mercury absorbed by people in industrial nations comes from their amalgam fillings.\

In 1991 the World Health Organization...... concluded the daily dose of mercury from the environment is 2.6 ug......... If the correct figure for absorption of mercury from amalgam turns out to be 8 ug, then the total mercury absorbed per day from all sources -- the environment plus amalgam -- is 10.6 ug, according to the WHO data. This means amalgam mercury constitutes three-fourths of all mercury absorbed by the body (8 ug is 75% of 10.6 ug). If 10 ug turns out to be the correct figure for mercury taken up from amalgams, then the total absorbed is 12.6, which means about four-fifths of all mercury absorbed comes from amalgams (10 ug is 79% of 12.6 ug).

In a 1995 report prepared for Health Canada (Canada's national health department), Richardson estimated that amalgam mercury constitutes half of the mercury absorbed daily by adult Canadians.

Whether amalgam mercury is the source of 50% of all mercury absorbed, as Richardson's data indicates, or three-fourths, as the WHO data suggests, mercury from amalgams contributes a substantial portion of the mercury absorbed each day, not a "very small" portion as the ADA would have the public believe.

Alzeimer’s symptoms and Mercury poisoning

A large body of research on the effect of accidental mercury poisoning indicates that mercury causes emotional and mental disturbances very similar to those that appear in many AD victims. Here is a summary of the emotional and mental symptoms commonly associated with AD: Patients with Alzheimer's exhibit changes in personality and social skills. They . . . may become socially uninhibited or lose all initiative and interest in activities. These patients often have delusions, hallucinations, and sleep disorders. They sometimes show grossly inappropriate judgment and sometimes are misdiagnosed as being depressed or psychotic.

Every one of these symptoms is common symptoms of mercury poisoning.

AD as an inflammatory response

The hypothesis that AD is caused by mercury from amalgam and the environment is consistent with the theory that AD is an inflammatory disease caused by the body's reaction to an infection or environmental insult. The evidence that AD "fits the paradigm of the idiopathic rheumatic disorders" was recently presented by Aisen and Davis.

"According to this model," wrote the authors, "an unknown set of circumstances results in an initial insult triggering an inflammatory reaction in the brain. The inflammation becomes self-propagating, or it continues because the obscure inciting factors persist." They argue that the acute phase response may augment production of beta-amyloid, the protein found among the plaques in AD brains. They conclude that "cytokines, acute phase proteins, activated microglia, and complement," all mechanisms which can be triggered by the acute phase response of the immune system, are "involved" with AD, either as causes or consequences, and that anti-inflammatory drugs may "alter" the progression of AD. Mercury may well be one of the "obscure inciting factors" that triggers the inflammatory response.

Some direct evidence that anti-inflammatory drugs may delay the onset of AD already exists. McGeer et al. reported data suggesting that "the prevalence of Alzheimer disease in patients with rheumatoid arthritis is unexpectedly low and that [the use of] anti-inflammatory therapy might be the explanation."

Sources and Additional Information:

http://www.robertgammal.com/PDFs/HgAlzheimers.pdf

http://www.nel.edu/pdf_/25_5/NEL240504R01_Mutter_.pdf

http://www.cancertutor.com/Alzheimers/Alzheimers.html

http://www.royalrife.com/flu_shots.html

http://www.hbci.com/~wenonah/hydro/amalgam.htm

http://www.thealzheimerssolution.com/?p=7

Head Injury - Risk Factor for Alzheimer's Disease

Although more than four decades have passed since British neurosurgeon McDonald Critchley described severe memory problems in a sample of boxers—presumably the result of repeated head trauma—the relationship between brain injury and Alzheimer's disease (AD) has proven difficult to unravel. For years, there was scant evidence that head injuries endured by nonboxers posed an increased risk for AD; although epidemiologic studies linking the two conditions began appearing in the 1980s, negative studies continue to be published with enough frequency to ensure that the issue remains controversial. And while recent reports have revealed neuropathologic changes in some injured brains that bear a remarkable resemblance to AD, the interpretation and implications of these findings remain uncertain.

Multiple researchers have overwhelming data that boxers have a high rate of dementia. Playing other sports where head injuries are common may also increase the risk of developing dementia, or perhaps cause it to develop at an earlier age. In an article published in NeuroSurgery in 2005, University of North Carolina scientists tested more than 2500 retired professional football players. They found those with three or more concussions were five times as likely to have Mild Cognitive Impairment and three times as likely to have significant memory problems compared to retirees without a history of concussion.

Nonetheless, some researchers believe that decoding the AD–brain injury connection will have implications far beyond the possibility of warding off dementia in head trauma patients. "It gives you insight into what may be the base mechanism for Alzheimer's disease," said Gareth W. Roberts, who coauthored several studies on the relationship between the two conditions before becoming Chief Executive Officer of the Cambridge, UK bioinformatics firm Proteom. "And once you have a feeling for what the core pathologic process is, you can ask, 'What kinds of things might stop that?'"

Other investigators envision similarly lofty applications. "I look upon head injury as a paradigm for understanding environmental risk factors for neurodegenerative diseases in general," said John Q. Trojanowski, Professor of Pathology and Laboratory Medicine at the University of Pennsylvania. For most patients, he noted, environmental factors are likely to far outweigh genetic influences in the etiology of neurodegenerative disease. "I think if we can 'crack' head trauma, it will open up ways of thinking about other environmental causes of these diseases."

WHAT HAPPENS AFTER BRAIN INJURY?

Recent studies have provided "very strong evidence that there is a connection between head trauma and at least some of the pathology of Alzheimer's disease," Dr. Trojanowski said. For example, in a report at the recent World Alzheimer Congress 2000, Steven T. DeKosky, and colleagues at the University of Pittsburgh Medical Center reported findings from neocortical samples taken from brain injury patients one and three days after injury. The samples, which were obtained by surgical resection and compared with postmortem samples from neurologically normal controls, revealed increases in amyloid precursor protein (APP), apolipoproteins E and D, and ß-amyloid (Aß). Many of the Aß deposits "had morphologic characteristics of classic amyloid plaques in AD," Dr. DeKosky and colleagues reported.

Several studies have found that Aß deposition occurs in a third of fatal head injury cases, even in children who survived only a few hours. The Aß is generally distributed throughout the brain; its presence does not correlate with cerebral contusions, increased intracranial pressure, or intracranial hematomas. Neurofibrillary tangles may also occur. The nature of pathology depends in part on injury severity—tangles do not seem to occur after mild trauma—but "I don't think there's much insight into how severe the injury has to be" to trigger AD-like pathology, Dr. Trojanowski said.

These changes make sense, Dr. Roberts said, if one accepts the view that Alzheimer's disease is largely an inflammatory process. APP is found in synapses, he noted, and "one of the things we do know happens after brain injury is synaptic remodeling." Moreover, electron microscopy shows that synapses are involved in amyloid plaque formation. This may be a repair process of some sort, he said, but "instead of being shut down when it is appropriate, it just carries on. It becomes a bit like arthritis, where mechanisms that should help you instead become chronically activated and disabling."

It should be noted, however, that the neuropathology of brain injury is by no means a carbon copy of the changes that occur in AD. For example, levels of growth inhibitory factor are increased in reactive astrocytes in experimentally induced brain injury, whereas these levels are reduced throughout the brain in AD. Moreover, the neocortical distribution of neurofibrillary tangles is more superficial in former boxers with dementia pugilistica, or punch drunk syndrome, than in AD patients.

HOW LARGE IS THE RISK?

Despite the array of pathologic evidence linking the disorders, the relationship between AD and head injury remains unsettled from an epidemiologic standpoint. Findings reported last year from the Rotterdam Study, for example, found no increased risk of AD in subjects with a history of head injury. Nonetheless, positive studies outnumber negative ones, and head injury is "becoming more accepted as being associated with the risk of AD," said Brenda L. Plassman, Director of the Program in Epidemiology of Dementia at Duke University Medical Center.

In a new report Dr. Plassman and colleagues performed telephone screening of more than 2,000 World War II veterans who had been hospitalized for head injury, pneumonia, or puncture wounds in 1944 or 1945. Subjects who screened positive for possible dementia underwent a three-hour exam that included neuropsychologic testing, neurologic examination, and DNA collection.

From 1940s armed forces hospital records, the researchers were able to estimate the severity of each subject's head injury, based on the occurrence of amnesia or skull fracture and the duration of unconsciousness. The findings revealed that "the more severe the injury, the greater the risk of AD and dementia"; the relative risks (compared with controls) ranged from about 2 for moderate head injury to 4 for severe injury. The findings are consistent with those from most other positive epidemiologic studies, Dr. Plassman said. "It's rather striking that all of these studies used different samples, methods, and criteria for head injury, yet all have odds ratios that are pretty close." The relative risk of AD after head injury is roughly similar to that reported for subjects heterozygous for the APOE*E4 allele, she added.

THE GENETIC CONNECTION

The role of genetic vulnerability is suggested by the fact that only a subset of brain injury patients develops amyloid pathology. Many investigators believe APOEgenotype is the key culprit. "There is a clear relationship between having an APOE*E4 allele and your likelihood of developing plaques after a head injury," Dr. Roberts said. "So in a sense the APOE–head injury story gives you the first genetic–environmental interaction in a neurologic disease." This relationship is consistent with APOE's proposed role in the maintenance and repair of neuronal membranes, synaptogenesis, and other processes. Indeed, researchers at the University of Glasgow reported earlier this year that the densities of the ß-amyloid peptides Aß-42 and Aß-40 in head injury patients were related in a dose-dependent manner to APOE*E4 endowment.

However, it is possible that in many cases head injury doesn't induce AD-like pathology so much as accelerate its arrival. A 1989 retrospective study found that a history of head injury was associated with earlier onset of AD. And a report from the Mayo Clinic suggested that AD rates were not elevated among subjects with a history of head trauma, but that the injury hastened the time to AD onset by about eight years.

FUTURE INTERVENTIONS

Can prompt, appropriate treatment after brain injury reduce or prevent the development of AD-like pathology? While the mouse model for AD that Dr. Trojanowski and others have been using has yielded interesting findings, the rodents' lack of tau pathology and "quirky" behavior did not allow for ideal testing of therapeutic interventions.

Until now, researchers have lacked a good animal model for studying the development of Alzheimer's disease. The transgenic mice used in the CNDR contain the human gene that produces the Ab protein. With the aid of techniques developed at the Penn Head Injury Center, Uryu and his colleagues were able to study how just mild repetitive head injuries could influence the progress of Alzheimer's disease.

Even without head trauma, these mice would eventually develop Ab plaques later in life. With the trauma, they produce symptoms of Alzheimer's disease at a remarkably increased rate.

"Here, we can clearly see a direct cause and effect relationship between repetitive concussions and Alzheimer's," said John Q. Trojanowski. "Using the head trauma model in these mice represents a step forward in our ability to understand the basic molecular mechanisms behind Alzheimer's disease. More importantly, we believe this model system can be used to screen for new medications in the search for a cure."

At present, "aside from telling football players and soccer players to either not play or to wear a helmet, there's not much in the way of interventions," Dr. Trojanowski noted. However, as researchers gain a better understanding of the relationship between trauma, risk factors, and genetic vulnerability, medical advice could theoretically be targeted to a patient's profile: "If you're APOE*E4 homozygous, you should really think twice about playing football. If you're heterozygous for APOE*E4, you'd better wear a helmet and take vitamin E and aspirin for the rest of your life."

Moreover, the inflammatory model of AD pathogenesis offers obvious potential for intervention. Epidemiologic studies have found a reduced rate of AD among people who regularly used nonsteroidal anti-inflammatory drugs. And a study in the Journal of Neurosciencefound that ibuprofen reduced not only inflammation, but Aß plaque burden in a transgenic mouse model for AD.

An interesting recent 2008 year study at Washington University in St. Louis and the University of Milan evaluated hour-by-hour measurements of the protein amyloid beta in 18 patients with severe brain injury as they were coming out of a coma.

"We were trying to understand why traumatic brain injury increases the risk of Alzheimer's disease," said Dr. David Brody of Washington University, who estimates that people with severe brain injuries have a two to four times greater risk of developing Alzheimer's disease.

The classic theory is that such injuries increase the amount of amyloid beta, which may accelerate the development of sticky clumps of amyloid plaque that is a hallmark of Alzheimer's disease.

To study the classic theory related to the increasing amount of amyloid beta, accelerating the development of sticky clumps of amyloid plaque, the teams placed a small catheter into the brains of the patients to sample fluid in the spaces between cells, where amyloid beta protein accumulates. Then, they took hourly measurements of the fluid to check levels of the protein.

"What we were expecting was that amyloid beta levels would be high immediately after the injury and fall over time," Brody said in a telephone interview. What they saw instead was a gradual increase in levels of this protein as patients recovered brain function. The better the patients got, the higher their amyloid beta levels rose. And in patients whose neurological function worsened, amyloid beta fell.

Brody said the finding suggests that amyloid beta in the human brain may be an indicator of how well brain cells are communicating, something studies in mice have suggested.

And while it also proves it is possible to directly measure amyloid beta in humans, "it raises a lot more questions than it answers," Brody said.

Sources and Additional Information:

http://www.neuropsychiatryreviews.com/oct00/npr_oct00_brain.html

http://www.reuters.com/article/healthNews/idUSPAT87667620080828

http://www.tangledneuron.info/the_tangled_neuron/2007/03/head_injuries_a.html

http://www.newscientist.com/article/dn12002-brain-injuries-unleash-alzheimers-threat.html

Confirmed Genetic Causes of Alzheimer's Disease

Alzheimer disease has a genetic cause in up to 80 percent of cases, according to a study of nearly 12,000 twin pairs from the Swedish Twin Registry at Karolinska Institutet.

Alzheimer's and Genetics


Perhaps the most investigated field of the new millennium is genetics. Diseases such as cystic fibrosis, muscular dystrophy, and Huntington's disease are single-gene disorders. If a person inherits the gene that causes one of these disorders, he or she will usually develop the disease.

Researchers have observed that having a parent or sibling with Alzheimer’s disease does increase one’s risk somewhat above the general population’s risk of developing the disease, but such a family history should not cause undue anxiety. Nonetheless, some people with such family histories, and some without such histories, wish to have a genetic test that will answer the question: Will I be next?

Alzheimer's disease, however, is not caused by a single gene, which makes the genetic link to the disease much more complication.

The Genetics of Alzheimer’s Disease

AD is an irreversible, progressive brain disease characterized by the development of amyloid plaques and neurofibrillary tangles, the loss of connections between nerve cells in the brain, and the death of these nerve cells. AD has two types: early-onset and late-onset. Both types have genetic links.

Early-Onset AD

Early-onset AD is a rare form of AD, affecting only about 5 percent of all people who have AD. It develops in people ages 30 to 60.

Some cases of early-onset AD, called familial AD (FAD), are inherited. FAD is caused by a number of different gene mutations on chromosomes 21, 14, and 1, and each of these mutations causes abnormal proteins to be formed. Mutations on chromosome 21 cause the formation of abnormal amyloid precursor protein (APP). A mutation on chromosome 14 causes abnormal presenilin 1 to be made, and a mutation on chromosome 1 leads to abnormal presenilin 2.

The chromosome 21 gene also intrigues Alzheimer's researchers because of its role in Down syndrome. People with Down syndrome have an extra copy of chromosome 21 and, as they grow older, usually develop abnormalities in the brain like those found in Alzheimer's disease.

Mutations in a gene called PS1 account for about half of all early onset Alzheimer's disease in families. Despite its importance in the disease, researchers do not know what role PS1 normally plays in the body.

Researchers have found more than 40 different mutations in the PS1 gene that cause early onset Alzheimer's disease in families of different ethnic backgrounds.

People with mutations in PS1 develop Alzheimer's disease at the earliest age, ranging from 29 to 62 but with an average age of 44 years. Families with a particular PS1 mutation tend to develop Alzheimer's at the same age.

In four families with mutations in PS1, those who develop Alzheimer's disease also have weakness in the legs and more extensive changes in their brains than most people with Alzheimer's disease.

The PS2 gene has a very similar sequence to the PS1 gene, and, like the PS1 gene, researchers do not know its normal role in the body. Mutations in the PS2 gene are very rare. In fact, mutations in this gene have only been found in six different families with Alzheimer's disease. One mutation accounts for Alzheimer's disease in five German families and the other is responsible for the disease in an Italian family.

Unlike the PS2 or APP genes, researchers have found people who have a mutation in the PS2 gene but did not develop Alzheimer's disease. This, and the longer duration of Alzheimer's disease in people with PS2 mutations, makes researchers think that mutations in PS2 cause a less aggressive form of Alzheimer's than in people with PS1 mutations. The age when people with PS2 mutation develop symptoms of Alzheimer's disease varies even in the same family, indicating that some environmental factors also influence when a person with a PS2 mutation develops the disease.

In general, even if only one of these mutated genes is inherited from a parent, there is a significant chance for person to develop early-onset AD. This inheritance pattern is referred to as “autosomal dominant” inheritance. In other words, offspring in the same generation have a 50/50 chance of developing FAD if one of their parents had it.

Scientists know that each of these mutations causes an increased amount of the beta-amyloid protein to be formed. Beta-amyloid, a major component of AD plaques, is formed from APP.

These early-onset findings were critical because they showed that genetics were involved in AD, and they helped identify key players in the AD process. The studies also helped explain some of the variation in the age at which AD develops.

Late-Onset AD

Most cases of Alzheimer’s are of the late-onset form, developing after age 60. Scientists studying the genetics of AD have found that the mutations seen in early-onset AD are not involved in this form of the disease.

Although a specific gene has not been identified as the cause of late-onset AD, one predisposing genetic risk factor does appear to increase a person’s risk of developing the disease. This increased risk is related to the apolipoprotein E (APOE) gene found on chromosome 19. APOE contains the instructions needed to make a protein that helps carry cholesterol in the bloodstream. APOE comes in several different forms, or alleles.

Three forms—APOE ε2, APOE ε3, and APOE ε4—occur most frequently.

• APOE ε2 is relatively rare and may provide some protection against the disease. If AD does occur in a person with this allele, it develops later in life than it would in someone with the APOE ε4 gene.
• APOE ε3 is the most common allele. Researchers think it plays a neutral role in AD—neither decreasing nor increasing risk.
• APOE ε4 occurs in about 40 percent of all people who develop late-onset AD and is present in about 25 to 30 percent of the population. People with AD are more likely to have an APOE ε4 allele than people who do not develop AD. However, many people with AD do not have an APOE ε4 allele.

Dozens of studies have confirmed that the APOE ε4 allele increases the risk of developing AD, but how that happens is not yet understood. These studies also have helped explain some of the variation in the age at which AD develops, as people who inherit one or two APOE ε4 alleles tend to develop AD at an earlier age than those who do not have any. APOE ε4 is called a risk-factor gene because it increases a person’s risk of developing AD. However, inheriting an APOE ε4 allele does not mean that a person will definitely develop AD. Some people with one or two APOE ε4 alleles never get the disease, and others who develop AD do not have any APOE ε4 alleles.

Scientists believe that four to seven other AD risk-factor genes exist and are using a new approach called a genome-wide association study (GWAS) to help speed the discovery process. Another possible risk-factor gene, SORL1, was discovered in 2007. This gene is involved in transporting APP within cells, and its association with AD has been identified and confirmed in three separate studies. Researchers found that when SORL1 is present at low levels or in a variant form, beta-amyloid levels increase and may harm neurons.

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

Update 04-27-12:

The existence of two forms of Alzheimer's—early- and late-onset—has long baffled scientists. Of the estimated five million Americans who suffer from Alzheimer's, only a few thousand are diagnosed with an early-onset form of the affliction, which affects people before the age of 65. This rare early-onset form is thought to be hereditary and scientists have associated multiple genetic mutations contributing to its occurrence. Late-onset Alzheimer's, although more common, has been the bigger mystery. One variant of the APOE gene-—sometimes known as the Alzheimer's gene—is linked to the late-onset disease. But the APOE gene, unlike dominant early-onset genes, does not determine whether a person will ultimately have dementia.

Now there's evidence that late-onset Alzheimer's has a genetic basis similar to that of early-onset Alzheimer's. By sequencing select genes associated with the latter, along with frontotemporal dementia, researchers at Washington University in Saint Louis and other institutions found that patients with late-onset Alzheimer's carry some of the same genetic mutations as those with the early-onset form. The evidence, released February 2012, bolsters the argument that the forms of Alzheimer's that appear at different life stages should be classified as the same disease. As to why the disease appears earlier in some cases, the scientists speculated that those patients diagnosed relatively early in life carry more genetic risk factors for the disease.

This study's use of rapid genetic sequencing, the authors noted, may provide a model for more precise identification of dementias. Within the study, the researchers identified patients who may have been misdiagnosed as having Alzheimer's; the genes of these patients suggested that they had another type of dementia. Given the heritable component, patients with a family history could be screened to detect and diagnose Alzheimer's early.

Sources and Additional Information:

http://www.nia.nih.gov/Alzheimers/Publications/geneticsfs.htm

http://www.webmd.com/alzheimers/guide/alzheimers-genetic

http://www.genetichealth.com/alz_genetics_of_alzheimers_disease.shtml

http://www.accessdna.com/condition/Alzheimer_s_Disease/31

http://medinfo.ufl.edu:8050/year1/humbehav/readingmat/gold-alzheimers_genes.pdf

http://ki.se/ki/jsp/polopoly.jsp?d=25844&a=8774&l=en&newsdep=25844
http://www.scientificamerican.com/article.cfm?id=cracks-in-the-plaques-mys