Alzheimer disease is the most common form of dementia, accounting for 50 to 80 percent of all dementia cases. Dementia involves memory loss and other impaired intellectual abilities, all of which interfere with everyday life. Though most people with Alzheimer disease are over 65 years, up to five percent have early-onset Alzheimer’s, which usually appears during the mid-40s or 50s.
Beta-amyloid is a peptide found in plaques in the brains of people with Alzheimer disease. For a long time, it has been thought that beta amyloid-played a causative role in the neural degeneration of the disease. This may be a mistaken belief, however, as highlighted by a recent Phase III clinical trial on the anti-amyloid drug semagacestat. Patients in this trial were expected to improve on this drug, which interferes with the production of gamma-secretase, the enzyme that produces beta-amyloid. Instead, the drug “did not slow disease progression and was associated with worsening of clinical measures of cognitions and the ability to perform activities of daily living,” according to a press release put out by the drug manufacturer, pharmaceutical giant Eli Lilly. The trial was stopped before completion.
As it turns out, beta-amyloid is an antimicrobial peptide, and is suggested to be secreted by the brain in self-defense against infectious pathogens, as David Perlmutter, M.D. stated at the Institute for Functional Medicine’s 20th Symposium this past summer. We know beta-amyloid plaque builds up in the brain in people with Alzheimer disease, but what if its presence was a self-defense mechanism rather than the actual root cause of Alzheimer’s?
In a recent study by researchers at Mass General Institute for Neurodegenerative Disease, we may have our answer. The researchers stated, “Rather than beta-amyloid acting as a sole independent initiator of neuroinflammation, our data raise the possibility that the peptide may be part of a response mounted by the innate immune system. An absence of the peptide may result in increased vulnerability to infection.”1
Two main pathogens are implicated as possible triggers of Alzheimer disease: Herpes simplex virus 1, the virus known for causing cold sores of the mouth, and found in about 90 percent of all adults; and Chlamydia pneumonia, the respiratory bacteria known to cause pneumonia.
In one study, the presence of anti-HSV IgM antibodies was found to be an even bigger risk factor for the development of Alzheimer disease than even the “Alzheimer’s gene” APOE4 allele.2 In describing how Herpes may lead to Alzheimer’s, the researchers state, “Recurrent reactivation of HSV might act as a potent stimulus to the brain microglia, increasing the level of cytokines and initiating a positive feedback cycle that gives rise to an increasing accumulation of pathological changes.”
DNA from HSV1 and from Chlamydia pneumoniae has been found in the brains of people with Alzheimer disease.3,4 HSV1 was found in specific areas affected by Alzheimer’s, and Chlamydia was actually cultured from brain samples taken from recently-deceased Alzheimer’s patients, indicating the virus was alive in the brain.
Chlamydia pneumonia is also known as the “heart attack” bacteria, found in the intraclavicular space/fluid between gums and teeth. The best prevention for this, incidentally, is the use of Plaquers dental floss; dental floss with a handle. When the bacterium is found, orthodontal work should be performed. People with high levels of hs C-reactive protein (a marker of inflammation in the body) are at particular risk for mouth infection with C. pneumoniae bacteria. C. pneumoniae is associated with heart disease because it is also commonly found in the soft plaques of people who die of acute heart attack.
Dr. Perlmutter recommends L-lysine and vitamin D3 supplementation, in addition to a diet high in lysine, which includes whole grains, fruits, vegetables, cheese, yoghurt and fish, and is low in tofu and other soy foods high in arginine. It is thought that activation of the virus, as with cold sore outbreaks, is a sign the virus might be active in other areas, like the brain. Preventing this may be helpful for people with Alzheimer’s.
So, why do people get infections in the first place, and why do these infections get activated? Well, lack of vitamin D, which is more common than most people realize, and uncontrolled blood sugar levels and insulin resistance, both triggered by a diet high in refined carbohydrates and sugar, are factors which affect both cellular and adaptive immunity, making us more prone to viral and bacterial infections.
It is important to note that there is much more to this story than infections. Alzheimer disease is a multifactorial “perfect storm” of triggers—usually inflammatory triggers—that interact and overlap, creating the final neurodegeneration of Alzheimer’s. Infectious triggers are just one small piece to this puzzle. For general protection against Alzheimer’s, remove sugar from the diet, reduce saturated fat intake, and incorporate vitamin D, omega-3 fish oil, pre- and probiotics, fiber and digestive enzymes. Be sure to sleep well, eliminate regularly, get plenty of exercise and be happy.
- Soscia SJ, et al., “The Alzheimer’s disease-associated amyloid beta-protein is an antimicrobial peptide.” PLoS One. 2010 Mar 3;5(3):e9505.
- Letenneur L, et al., “Seropositivity to herpes simplex virus antibodies and risk of Alzheimer’s disease: a population-based cohort study.” PLoS One. 2008;3(11):e3637.
- Itzhaki RF and Wozniak MA, “Herpes simplex virus type 1 in Alzheimer’s disease: the enemy within.” J Alzheimers Dis. 2008 May;13(4):393-405.
- Gerard HC, et al., “Chlamydophila (Chlamydia) pneumoniae in the Alzheimer’s brain.” FEMS Immunol Med Microbiol. 2006 Dec;48(3):355-66.