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Alzheimer's, Dementia & Mental Health
Reduced Blood Flow Noted by Alois Alzheimer is Focus
of New Research
Changes to blood vessels had been pushed into
background of Alzheimer's research
 January 22, 2007 - The two dominant proteins that
determine how much blood flows through the body's arteries have been
implicated in Alzheimer's disease, in a new study in the Jan. 16 issue
of the Proceedings of the National Academy of Sciences. The researchers
say it offers new, surprising targets against Alzheimer's disease just as
scientists are getting back in touch with the vascular roots of the
disease that were first recognized early last century by Alois
Alzheimer.
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Alzheimer's, Dementia & Mental Health |
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The research, putting proteins often linked to
heart disease front and center in a brain disease whose causes remain a
mystery, hark back to what German physician Alzheimer noted when he
first recognized the disease 100 years ago.
Though Alzheimer noted changes in both the brain's
cells and in the small arteries and capillaries that supply and drain
blood to and from the brain, over the decades doctors separated the two
concepts and have come to focus mainly on the toxic effects of the
disease on cells. The changes to blood vessels have been pushed to the
background.
The latest findings from the University of
Rochester Medical Center mesh not only with Dr. Azheimer's initial
observations but also with new findings from today's best imaging
technologies.
While the first visible symptom of Alzheimer's may
be a person forgetting names or faces, the very first physical change is
actually a decline in the amount of blood that flows in the brain.
Doctors have found that not only is blood flow within the brain reduced,
but that the body's capacity to allocate blood to different areas of the
brain on demand is blunted in people with the disease.
"A reduction in blood flow precedes the decline in
cognitive function in Alzheimer's patients," said Berislav Zlokovic,
M.D., Ph.D., professor in the Department of Neurological Surgery and a
neurovascular expert whose research is causing scientists to consider
the role of reduced blood flow in Alzheimer's disease.
"People used to say, well, the brain is atrophying
because of the disease, so not as much blood as usual is needed. But
perhaps it's the opposite, that the brain is dying because of the
reduced blood flow," he added.
The new findings are the product of a five-year
collaboration between two types of scientists that traditionally don't
work closely together: neuroscientists who focus on the brain, and
cardiovascular experts who put most of their focus on the heart.
The first step in the study came when Zlokovic's
team compared the activity of genes in the brain from several people
with Alzheimer's who had died, to that of several people without the
disease who had died. It's a type of study widely done now by scientists
looking at a host of diseases, using vast gene arrays that can tell how
active thousands of genes are in a part of the body.
As Zlokovic perused the list of genes whose
activity differed depending on whether the person had Alzheimer's or
not, he recognized that several play a role in constricting the
arteries. He asked colleague Joseph Miano, Ph.D., a cardiovascular
researcher and expert on the smooth muscle that makes up part of the
arteries, to take a look.
Miano recognized the group as genes that are all
controlled by one of two master regulators of gene activity in smooth
muscle cells.
Proteins, myocardin and SRF (serum response
factor) exert control on blood vessel walls
Those proteins, myocardin and SRF (serum response
factor), are well known for the control they exert on blood vessel
walls. Working together, the two are the chief players that regulate how
much the smooth muscle cells inside the arteries contract. The more the
cells contract, the narrower the artery becomes, and the less blood that
flows.
In a series of experiments carried out together by
Miano's and Zlokovic's students and colleagues, the teams demonstrated
the power of the genes in the brain.
First they confirmed that both genes are more
active in the brains of Alzheimer's patients than they are in the brains
of people without the disease. They also found that when SRF or
myocardin are more active than usual in human smooth muscle tissue from
the brain, the muscle contracts more than usual.
In mice they found that when the genes were more
active than usual, blood flow in the brain was reduced, much like it is
in Alzheimer's disease in people. And finally, the scientists found that
when they silenced SRF, the phenomenon was reversed, and blood flowed
more freely.
While the two genes are widely known to
cardiovascular researchers like Miano, they're not studied much in the
Alzheimer's community. One study by Columbia University researchers last
year did find that SRF seems to play a role in learning and memory, but
its role in Alzheimer's has not been explored.
"This is fresh and exciting work," said Miano, an
expert on smooth muscle and associate professor of Medicine in the
Cardiovascular Research Institute. "For many vascular biologists, blood
flow in the brain is an afterthought, if that."
All this activity takes place in the smooth muscle
that lines most of the 60,000 miles of blood vessels that wind their way
through our bodies. SRF and myocardin control dozens of proteins that,
when overactive, pull the muscle tightly, constricting arteries and
reducing the amount of blood that can flow through them.
A similar type of muscle also lines our airways.
When smooth muscle there stays constricted too long, the result can be
asthma, since not enough air is getting to the lungs.
Now the group is looking for ways to stop the two
proteins from working together to constrict the blood vessels, so that
blood flow in the brains of people with Alzheimer's disease would return
to normal, much as the team achieved in mice.
"More and more, people are paying attention to the
role of the vascular system in Alzheimer's disease," said Zlokovic,
director of the Frank P. Smith Laboratories for Neurosurgical Research,
who has made several findings that implicate blood flow and the
blood-brain barrier transport mechanism as key components of the
Alzheimer's disease process.
The technology has been licensed to Socratech, a
Rochester biotech company created by Zlokovic to search for new
treatments for Alzheimer's and stroke. Miano has served as a consultant
to Socratech and is now leading a research effort there looking for
compounds to inhibit SRF and myocardin.
Editor's Notes
The first authors of the PNAS paper, who did most
of the laboratory work that led to the discovery, are Nienwen Chow,
Ph.D., a scientist at Socratech; graduate student Robert Bell; Rashid
Deane, Ph.D., associate professor of Neurological Surgery; and Jeffrey
Streb, Ph.D., a former graduate student in Miano's laboratory who is now
a post-doctoral researcher at UCLA. Other authors, in addition to
Zlokovic and Miano, include researcher Jiyuan Chen; Andrew Brooks,
Ph.D., of Rutgers University; and William Van Nostrand of Stony Brook
University.
The work was funded by the National Institute on
Aging, the National Heart Lung and Blood Institute, the American Heart
Association, and Socratech.
>>
University of Rochester Medical Center
>>
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