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Better Alzheimer’s Drugs May Come from Discovery
Anti-inflammatory function of Alzheimer's disease
drugs revealed
July 28, 2005 - The mechanism in anti-Alzheimer's
disease drugs that inhibits the production of a destructive,
inflammation-causing protein in the brain has been revealed by
researchers at the Hebrew University of Jerusalem, who say it could lead
to better treatment drugs.
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Their work, described in a recent issue of the
American journal, Annals of Neurology, is likely to lead to the
development of more efficient drugs than are currently in use for
treating Alzheimer's Disease as well as other neurological conditions
resulting from infections, autoimmune diseases such as multiple
sclerosis, or brain inflammation resulting from trauma or stroke.
Alzheimer's Disease is a degenerative disease of
the brain, characterized by a deterioration of both cognitive and
physical abilities. It first affects memory and the ability to carry out
complex, coordinated tasks. It also can bring on depression, inattention
and outbursts of anger. In a more progressive stage, the disease can
cause difficulties in the ability to perform even simple tasks such as
speaking and comprehending, eating and sleeping. The affected person can
even forget his name and identity.
The medicines administered today to Alzheimer's
Disease patients focus on preventing the breakdown of acetylcholine, a
chemical produced by brain cells which transmits information within the
brain and is vitally involved in cognitive processes that include
memory, attention and thought. Because acetylcholine-producing cells are
among the first to die in Alzheimer's Disease patients, drug-induced
elevation of acetylcholine levels partially attenuates the cognitive
deterioration.
In recent years it has been shown that another
pathological process that occurs in the brain of Alzheimer's Disease
patients is excessive immune activation and inflammation, which are
induced by overproduction of an inflammation-producing protein called
interleukin-1, as well as a few other related compounds. This process
can impair the functioning of nerve cells and can even lead to their
death. Furthermore, genetic alterations in the interleukin-1 gene have
been associated with increased risk for the appearance and severity of
Alzheimer's Disease symptoms.
The Hebrew University researchers found that
anti-Alzheimer's Disease drugs currently in use not only block the
activity of the enzyme responsible for breaking down acetylcholine but
also cause a marked reduction in the production of interleukin-1.
Furthermore, they describe the use of a novel drug (EN101), developed by
Prof. Soreq's team, which produces these effects in a more efficient way
than known heretofore by destroying the molecular antecedent (messenger
RNA) of the enzyme, rather than simply blocking the enzyme's activity.
In a series of experiments, conventional
anti-Alzheimer's Disease drugs, as well as the novel drug EN101, were
injected into mice with brain inflammation. It was found that these
injections reduced significantly the activity of the enzyme that breaks
down acetylcholine and blocked almost entirely the production of
interleukin-1.
The research team working on this project was
headed by Prof. Raz Yirmiya of the Psychology Department at the Hebrew
University, Dr. Yehuda Pollak, a post-doctoral fellow in Prof. Yirmiya's
laboratory; and in cooperation with Hermona Soreq, the Charlotte
Slesinger Professor of Cancer Studies at the Silberman Institute of Life
Sciences at the Hebrew University, and Prof. Tamir Ben-Hur of the Hebrew
University Faculty of Medicine.
"These findings suggest a new role for
acetylcholine in the brain," said Prof. Yirmiya. "When the
anti-Alzheimer's Disease drugs block the enzyme which breaks down
acetylcholine, the level of this chemical in the brain goes up, and
there is a reduction of the production of the inflammatory material,
interleukin-1, and its destructive influence in the brain."
"The discovery of this mechanism in the
anti-Alzheimer's Disease medicines points the way towards development of
new forms of these medicines which will block even more efficiently and
specifically the inflammatory and destructive activity of inteleukin-1,"
Prof. Yirmiya stressed. "Beyond that, it is likely that the drugs that
are currently used for treatment of Alzheimer's Disease, and
particularly the new drug EN101, will also be effective in dealing with
other inflammatory illnesses."
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