Alzheimer’s study points finger of blame at immune
Search for treatment, cure seems headed in new
direction today after Duke study
15, 2015 – The search for a cure or treatment of Alzheimer’s disease
appears to being going in a new direction today. New research points the
finger of blame away from "plaques" and "tangles" and toward a failure
of the immune system.
A Duke University study published in the Journal
of Neuroscience found that cells in the immune system that normally
protect the brain from infection will begin to consume a key nutrient,
arginine, during the early stages of Alzheimer’s.
The researchers blocked this process in lab mice
with a small-molecule drug, difluoromethylornithine (DFMO), which
prevented the brain plaques and the loss of memory. This stopped the
damage caused by arginase, an enzyme which breaks down arginine.
“Plaques and tangles in the brain are two of the
main features of Alzheimer’s disease,” according to the
National Institute on Aging. “The third is the loss of connections
between nerve cells (neurons) in the brain.”
Oral vaccine targets RAGE and amyloid by using body's immune system
Sept. 26, 2011 – An accomplice to the protein that causes plaque buildup in Alzheimer's disease is the focus of a
potential new treatment, according to research by a Georgia Health Sciences University graduate student.
Alzheimer’s is an irreversible, progressive brain
disease that slowly destroys memory and thinking skills and, eventually
even the ability to carry out the simplest tasks of daily living.
In most people with Alzheimer’s, symptoms first
appear after age 65. Alzheimer’s disease is the most common cause of
dementia among older people. There are about 5 million cases
in the U.S. today.
The mystery is not completely solved, however, as
the precise role of the immune system cells is not understood. Still,
the study points to a new possible cause of AD, which could open the
door to new therapy.
"If indeed arginine consumption is so important to
the disease process, maybe we could block it and reverse the disease,"
said Carol Colton, professor of neurology at the Duke University School
of Medicine, a senior author of the study.
"We see this study opening the doors to thinking
about Alzheimer's in a completely different way, to break the stalemate
of ideas in Alzheimer's disease."
Research into the brains of Alzheimer's sufferers
has typically focused on plaques and tangles. Plaques are a build-up of
sticky proteins known as beta amyloid while tangles are a twisted
protein called tau.
By studying a type of mouse created several years
ago with a similar type of immune system to a human, researchers found
that immune cells called microglia began to divide and change early in
the onset of Alzheimer's.
"All of this suggests to us that if you can block
this local process of amino acid deprivation, then you can protect - the
mouse, at least - from Alzheimer's disease," said Matthew Kan, one of
the researchers involved in the study.
The researchers will next test older mice that
already have an advanced form of Alzheimer’s.
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