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This excerpt taken from the ELN 20-F filed Feb 26, 2009. Our
Scientific Approach
Our scientific approach to Alzheimer’s disease is centered
upon landmark basic research that revealed that a toxic protein
called beta amyloid (or abeta 1-42, or Aß) accumulates in
the brains of people with Alzheimer’s disease. The process
by which this protein is generated, aggregates and is ultimately
deposited in the brain as plaques is often referred to as the
amyloid cascade. The formation of beta amyloid plaques is a
hallmark pathology of Alzheimer’s disease.
A growing body of scientific evidence, discovered by researchers
at Elan and other organizations, indicates that modulating the
amyloid cascade may result in the successful treatment of
Alzheimer’s disease patients, by attacking the underlying
disease process.
Beta amyloid forms when a small part of a larger protein called
the amyloid precursor protein (APP) separates from the larger
protein. This separation happens when enzymes called secretases
“clip” (or cleave) APP. It is
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becoming increasingly clear that once beta amyloid is produced,
it exists in multiple physical forms (or “species”)
with distinct functional activities. It is believed that the
toxic effects of some of these forms are likely responsible for
the complex cognitive, functional and behavioral deficits
characteristic of Alzheimer’s disease.
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