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This excerpt taken from the ELN 20-F filed Feb 28, 2007. Our
Scientific Approach to Alzheimer’s Disease and Related
Disorders
Our scientific approach to treating Alzheimer’s disease
focuses on the beta amyloid hypothesis, as it is believed that
blocking the generation of beta amyloid in the brain or
enhancing the clearance of beta amyloid will result in the
successful treatment of Alzheimer’s disease patients. The
beta amyloid hypothesis asserts that beta amyloid is involved in
the formation of the plaque that causes the disruption of memory
and cognition that is the hallmark of Alzheimer’s disease.
This hypothesis is also the leading approach to developing
therapeutic treatments that may fundamentally alter the
progression of the disease, and evidence suggests that clearance
of beta amyloid may lead to improved function in
Alzheimer’s disease patients.
Beta amyloid, also known as Abeta, is actually a small part of a
larger protein called the amyloid precursor protein (APP). Beta
amyloid is formed when certain enzymes called secretases
“clip” (or cleave) APP. It is becoming increasingly
clear that once beta amyloid is released, it exists in multiple
physical forms with distinct functional activities. It is
believed that the toxic effects of these forms are likely
responsible for the complex mental disruption characteristic of
Alzheimer’s disease.
Table of Contents
This excerpt taken from the ELN 20-F filed Mar 30, 2006. Our
Scientific Approach to Alzheimer’s Disease and Related
Disorders
Our scientific approach to treating Alzheimer’s disease
focuses on the beta amyloid hypothesis, as it is believed that
blocking the generation of beta amyloid in the brain or
enhancing the clearance of beta amyloid will result in the
successful treatment of Alzheimer’s disease patients. The
beta amyloid hypothesis asserts that beta amyloid is involved in
the formation of the plaque that causes the disruption of
thinking that is the hallmark of Alzheimer’s disease. This
hypothesis is also the leading approach to developing
therapeutic treatments that may fundamentally alter the
progression of the disease, and evidence suggests that clearance
of beta amyloid may lead to improved function in
Alzheimer’s disease patients.
Table of Contents
Beta amyloid, also known as Abeta, is actually a small part of a
larger protein called the amyloid precursor protein, or APP.
Beta amyloid is formed when certain enzymes called secretases
“clip” (or cleave) APP. It is becoming increasingly
clear that once beta amyloid is released, it exists in multiple
physical forms with distinct functional activities. It is
believed that the toxic effects of these forms are likely
responsible for the complex mental disruption characteristic of
Alzheimer’s disease.
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