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Topic: Research Points To Link Between The Herpes (HSV1) Virus & Alzheimer's Disease...Vaccine Treatment Possible!!

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Research Points To Link Between The Herpes (HSV1) Virus & Alzheimer's Disease...Vaccine Treatment Possible!!

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Last week an advisory committee to the Food and Drug Administration unanimously recommended the approval of a diagnostic brain scan for Alzheimer's disease. The new technology is based upon imaging and quantifying the amount of a specific protein, beta amyloid, in the brains of patients suspected of having the disease. Research has demonstrated a striking correlation between the amount of beta amyloid in the brain and the degree of cognitive impairment in Alzheimer's patients.

Dr. Norman Foster, professor of neurology at the University of Utah, testified before the FDA committee and was quoted in The New York Timesstating the approval of the new scan "would be a historic advance in neurology and in the daily management of patients with memory complaints," an interesting comment as the article goes on to say, "If a person has Alzheimer's though, there is as yet no treatment that can slow or reverse the disease ... "

Assuming beta amyloid is produced in response to an infectious agent, logically we would want to examine the evidence supporting the role of infection in Alzheimer's disease. Over the past several years, compelling evidence has surfaced linking herpes simplex virus type 1 (HSV1) to Alzheimer's disease.

In 2008, Canadian researchers Luc Letenneur and Karine Peres demonstrated a dramatic increase in antibodies directed against HSV1 in Alzheimer's patients compared to age-matched individuals without the disease. Professor Ruth Itzhaki from the University of Manchester has explored the relationship of HSV1 to Alzheimer's disease in great depth.

In her landmark article published in 2008 entitled "Herpes Simplex Virus Type 1 in Alzheimer's disease: The Enemy Within," Dr. Itzhaki revealed that HSV1 infects the brains of 90 percent of adults. If HSV1 causes Alzheimer's, this high rate of infection would be a necessary characteristic in light of the very high prevalence of Alzheimer's disease.

Further, she points out, HSV1 can remain latent in the nervous system lifelong and may undergo periodic reactivation causing persistent brain inflammation. As an example, HSV1 is the cause of recurrent fever blisters that occur when the virus gets activated in the brain. Undoubtedly the most compelling evidence linking HSV1 to Alzheimer's disease comes from her recent discovery of HSV1 DNA actually located exactly within the beta amyloid plaque, the so-called "hallmark" of the disease.

So compelling are these findings that Dr. Itzhaki has concluded, "Our present data suggest that this virus is a major cause of amyloid plaques and hence probably a significant etiological factor in Alzheimer's disease. They point to the usage of antiviral agents to treat the disease and possibly of vaccination to prevent it."

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