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New Genetic Cause of Alzheimer's Found
Study
says quantity of amyloid protein is key to early dementia
April 19,2006 - Researchers from Belgium are today
claiming to be the first to show that the quantity of amyloid protein in
brain cells is a major risk factor for Alzheimer's disease. Amyloid
protein has been known to be the primary component of the senile plaques
in the brains of patients. The new discovery demonstrates that the
greater the quantity of the protein that is produced, the younger the
patient is when dementia develops.
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The researchers are from the Flanders
Interuniversity Institute for Biotechnology (VIB), which is connected to
the University of Antwerp in Belgium.
Alzheimer's disease
Alzheimer's disease is a memory disorder that affects up to 70% of all
dementia patients. The disease gradually destroys brain cells in the
deep areas of the brain that are responsible for memory and knowledge.
Ever since the disease was first reported by Alois Alzheimer − 100 years
ago − scientists have been searching diligently for ways to treat it.
Amyloid plaque formation plays a key role
Genetic research has previously shown a direct connection between
amyloid protein and the development of senile plaques and loss of cells.
Amyloid protein originates when it is cut by enzymes from a larger
precursor protein.
In very rare cases (fewer than 1 in 1000 patients),
mutations appear in that amyloid precursor protein, causing it to change
shape and be cut differently. The amyloid protein that is formed now has
different characteristics, causing it to begin to stick together and
precipitate as amyloid plaques. The development of amyloid plaques in
the brain tissue of Alzheimer patients is a central factor in the search
for a therapy for Alzheimer's disease.
A lot or not much of the amyloid precursor protein
is a risk factor The fact that patients with Down syndrome get
Alzheimer's disease shows that the quantity of the amyloid precursor
protein contributes to the disease: in fact, patients with Down syndrome
have 3 copies of the gene (or hereditary code) for the amyloid precursor
protein and therefore produce 150% instead of 100% of the protein.
So, Jessie Theuns and her colleagues, under the
direction of Christine Van Broeckhoven, hypothesized that the quantity
of amyloid precursor protein might also play a role in Alzheimer's
disease. The geneticists from Antwerp systematically studied the
hereditary code that is responsible for controlling the expression of
the gene.
Biological processes in human bodies are strictly
regulated, primarily by closely controlling the amount of each protein
that is produced. The promoter of a gene has the most important control
function in this process.
In younger Belgian and Dutch Alzheimer's patients
(younger than 70), the researchers found genetic variations in the
promoter that increased the gene expression and thus the formation of
the amyloid precursor protein.
These variations in the promoter that increase
expression occur up to 20 times more frequently (2 per 100 patients)
than the mutations in the precursor protein that change the shape.
Furthermore, there is a connection with the age at which the symptoms
are first detected: the higher the expression (up to 150% as in Down
syndrome), the younger the patient (starting between 50 and 60 years of
age). Thus, the amount of amyloid precursor protein is a genetic risk
factor for Alzheimer's disease in the aging process.
Prospects for tests and treatments
These new findings, the researchers say, lead to a new understanding:
namely, that the quantity of the amyloid precursor protein, and thus of
the amyloid protein, in brain cells contributes significantly to the
risk of contracting Alzheimer's. This discovery will have to be taken
into account in diagnostic tests and in the search for new medicines,
they say.
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