Herpes and Alzheimers

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Source: Brown University <http://www.brown.edu/Administration/News_Bureau>

Date: November 7, 2003

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Herpes Research Uncovers Possible Clue To Alzheimer's Disease

Providence, R.I. -- Researchers at Brown University and the Marine

Biological Laboratory at Woods Hole, Mass., have found a physical

connection between the herpes simplex virus and amyloid precursor

protein, a protein that breaks down to form a major component of the

amyloid plaques that are consistently present in the brains of persons

with Alzheimer's disease.

------------------------------------------------------------------------

Amyloid precursor protein or APP breaks down to form beta-amyloid. There

is strong evidence, according to the researchers, that beta-amyloid is

the underlying cause of Alzheimer's.

While the scientists caution that no conclusions about Alzheimer's can

be drawn from their findings, Dr. Elaine Bearer, senior research

scientist and associate professor in Brown's Department of Pathology and

Laboratory Medicine, believes the work does in fact link the common

herpes virus of cold sores with the neurodegenerative disorder. Bearer

isalso a summer investigator at the Marine Biological Laboratory at

Woods Hole, Mass.

Past studies have implicated the herpes virus in the onset of

Alzheimer's disease, but agreement within the scientific community on

the value of that research is far from universal. Bearer expects that

the discovery of a physical interaction between APP and the herpes virus

will trigger further investigations into the role the virus may play in

the disease, and even into possible uses of the virus in therapy.

The scientists stress that none of what they found should cause alarm

among those who have at one time had a cold sore. According to Bearer,

nearly 85 percent of us harbor the herpes simplex virus and most of us

never develop Alzheimer's.

The researchers discovered the interaction between the herpes simplex

virus (HSV) and APP while conducting experiments in the giant axon of

squid at the Marine Biological Laboratory. Prasanna Satpute-Krishnan and

ph A. DeGiorgis, both doctoral candidates in Brown's graduate

program at the time of the research, were seeking to learn how viruses

are carried around the body within cells and from one cell to another.

Specifically, they were examining how the herpes simplex virus travels

back to the lip area to form a recurring blister after remaining latent

for some time in the trigeminal ganglion, a collection of nerve cells

next to the brain.

What they found was that the herpes virus was interacting with APP, a

putative motor receptor that recruits a microtubular motor, kinesin, for

transport through neurons. This was the first time scientists had

observed any physical interaction between the herpes virus and APP.

Without the APP, the virus moves backward up an axon (a long extension

of a neuron) from the area of the lip towards the trigeminal ganglion.

But the Brown researchers discovered that once it interacts with the

APP, the virus travels in the opposite direction what scientists

describe as anterograde transport back down to the lip. The researchers

also found that once coupled with the APP, the virus moves remarkably fast.

" It's as if the virus hijacks a car which in this case would be the

kinesin and the APP is the driver, " explains Bearer. " The virus takes

the APP where it wants to be, not where the APP wants to be. "

The build-up of beta-amyloid (formed in the breakdown of APP) is found

consistently in the brains of Alzheimer's patients, and many scientists

are now convinced it is involved in the disease, according to

Satpute-Krishnan. Questions persist, however, as to what that

involvement is, and why, when APP is found in all of us, it causes

problems only in a few.

Perhaps, Bearer speculates, when the APP is co-opted by the herpes

virus, the APP breaks down at a location where it would not normally

appear and at a very different rate. " When APP piles up around neurons,

the neurons die, " she explains. " But we don't yet know if this is a

secondary or a primary cause of Alzheimer's. "

" At this point, of course, we don't yet know whether herpes plays a

causal role in Alzheimer's disease, " DeGiorgis notes. " But our research

does provide some interesting new insight into both diseases. "

A paper outlining the findings of the Brown/MBL researchers titled " Fast

Anterograde Transport of Herpes Simplex Virus: Role of Amyloid Precursor

Protein " will appear in the December issue of Aging Cell, published by

Blackwell Publishing in England and at the publisher's " OnlineEarly "

site [http://www.blackwell-synergy.com/links/toc/ace].

Satpute-Krishnan, the first author of the paper, is a graduate student

in Brown's Molecular Biology, Cell Biology and Biochemistry Graduate

Program. Bearer, who holds both an M.D. and a Ph.D., is an experimental

pathologist. DeGiorgis, who earned his Ph.D. in Bearer's lab last year,

is now with the National Institutes of Health.

Experiments in this study were conducted in the giant axon of squid, a

model widely used in research because with a diameter of nearly a

millimeter it is 1,000 times thicker than a human axon. Researchers are

able to inject substances into the giant axon and then observe the

behavior of those substances through high-powered microscopes.

" It is pretty extraordinary that breakthroughs in Alzheimer's disease

and in the pathogenesis of herpes virus should be made using the squid

of the North Atlantic sea, " notes Bearer.