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Alzheimer's And Herpes Simplex Virus: A Link?

http://www.huffingtonpost.com/dr-david-perlmutter-md/alzheimers-herpes-could-be-\

a-cause_b_814047.html

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 , professor of neurology at the University of Utah, testified

before the FDA committee and was quoted in The New York Times stating 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 ... "

Over the past several decades, the understanding of beta amyloid's role as a

causative agent for Alzheimer's disease has served to underpin worldwide

research in attempt to develop meaningful treatments designed to rid the brain

of this damaging protein. Interestingly, these attempts have met with almost

universal failure. Most recently, pharmaceutical giant Eli Lilly announced yet

another failure in an attempt to chemically reduce beta amyloid in humans. In an

August 17, 2010 press release the company noted that their experimental drug

semagacestat, an " oral agent designed to reduce the body's production of amyloid

beta plaques, which scientists believe play an important role in causing

Alzheimer's disease, " actually caused more rapid decline in Alzheimer's

patients. The company revealed that patients treated with the experimental drug

" worsened to a significantly greater degree than those treated with placebo. "

If beta amyloid were the cause of Alzheimer's disease, then why would ridding

the brain of this protein actually cause patients to worsen? Harvard researcher

Dr. Soscia and her associates may have the answer. Their recently

published research questioned why beta amyloid accumulates in the Alzheimer's

brain in the first place, and concluded that in fact, the protein actually

serves to rid the brain of a variety of bacteria and viruses. They described

beta amyloid as an " antimicrobial peptide " which accumulated in response to an

infectious agent. Their work looks upon beta amyloid in a new light as they

stated, " If the normal function of beta amyloid is to function as an

antimicrobial peptide, then an absence of the peptide may result in increased

vulnerability to infection. " Rather than causing the disease, beta amyloid may

be our brain's natural response to an infectious agent, accumulating as a way of

defending us against a pathogen. So perhaps we should reconsider beta amyloid

since it has been said that " the enemy of my enemy is my friend. "

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. "

The FDA's likely approval of technology allowing the quantification of beta

amyloid in suspected Alzheimer's patients will clearly provide a valuable tool

in defining the cause of dementia in cognitively impaired individuals. But

focusing on ridding the brain of this protein may be treating the smoke while

ignoring the fire. Indeed, the evidence now suggests that beta amyloid protein

may very well represent a positive response in the brain's attempt to deal with

a viral infection. Proving the role of HSV1 in Alzheimer's disease could be as

simple as treating a group of patients with readily available antiviral

medication. Dr. Itzhaki recently sent me an email indicating she stands ready to

get this research underway, but as is so often the case, funding the study

remains a challenge.

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Thanks for posting this.  Would you happen to know if the HSV 1 virus is also

connected to primary amyloidosis?  Amyloidosis is the build up of light chain

amyloid protein deposits in the organs. I have looked but did not find an

answer, I will have to do more digging when I have more time. 

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  • 2 weeks later...

This is all very interesting. We have been exploring antiviral therapy for my

son and it seems to be having a HUGE effect. There was a post on here a month

or so ago aout a doctor in CA that feels that many of the problems with children

with special needs is that they are viral. It has a big key for us.

>

> Alzheimer's And Herpes Simplex Virus: A Link?

>

http://www.huffingtonpost.com/dr-david-perlmutter-md/alzheimers-herpes-could-be-\

a-cause_b_814047.html

>

> 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 , professor of neurology at the University of Utah, testified

before the FDA committee and was quoted in The New York Times stating 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 ... "

>

> Over the past several decades, the understanding of beta amyloid's role as a

causative agent for Alzheimer's disease has served to underpin worldwide

research in attempt to develop meaningful treatments designed to rid the brain

of this damaging protein. Interestingly, these attempts have met with almost

universal failure. Most recently, pharmaceutical giant Eli Lilly announced yet

another failure in an attempt to chemically reduce beta amyloid in humans. In an

August 17, 2010 press release the company noted that their experimental drug

semagacestat, an " oral agent designed to reduce the body's production of amyloid

beta plaques, which scientists believe play an important role in causing

Alzheimer's disease, " actually caused more rapid decline in Alzheimer's

patients. The company revealed that patients treated with the experimental drug

" worsened to a significantly greater degree than those treated with placebo. "

>

> If beta amyloid were the cause of Alzheimer's disease, then why would ridding

the brain of this protein actually cause patients to worsen? Harvard researcher

Dr. Soscia and her associates may have the answer. Their recently

published research questioned why beta amyloid accumulates in the Alzheimer's

brain in the first place, and concluded that in fact, the protein actually

serves to rid the brain of a variety of bacteria and viruses. They described

beta amyloid as an " antimicrobial peptide " which accumulated in response to an

infectious agent. Their work looks upon beta amyloid in a new light as they

stated, " If the normal function of beta amyloid is to function as an

antimicrobial peptide, then an absence of the peptide may result in increased

vulnerability to infection. " Rather than causing the disease, beta amyloid may

be our brain's natural response to an infectious agent, accumulating as a way of

defending us against a pathogen. So perhaps we should reconsider beta amyloid

since it has been said that " the enemy of my enemy is my friend. "

>

> 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. "

>

> The FDA's likely approval of technology allowing the quantification of beta

amyloid in suspected Alzheimer's patients will clearly provide a valuable tool

in defining the cause of dementia in cognitively impaired individuals. But

focusing on ridding the brain of this protein may be treating the smoke while

ignoring the fire. Indeed, the evidence now suggests that beta amyloid protein

may very well represent a positive response in the brain's attempt to deal with

a viral infection. Proving the role of HSV1 in Alzheimer's disease could be as

simple as treating a group of patients with readily available antiviral

medication. Dr. Itzhaki recently sent me an email indicating she stands ready to

get this research underway, but as is so often the case, funding the study

remains a challenge.

>

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