Alzheimer's, Dementia & Mental Health
Potentially Powerful Tool in Battle Against
Alzheimer’s Disease Discovered at Mayo
Enzyme destroys beta-amyloid found in brains of
those with the disease
Sept. 17, 2012 - An enzyme (protein that controls
biochemical reactions) that could represent a powerful new tool for
combating Alzheimer's disease
has been discovered by researchers at
Mayo Clinic in Florida. This
protein - known as BACE2 - destroys beta-amyloid, a toxic protein
fragment that litters the brains of patients who have the disease. The
findings were published online today in the science journal
Alzheimer's disease is the most common memory
disorder. It affects more that 5.5 million people in the United States.
Despite the disorder's enormous financial and personal toll, effective
treatments have not yet been found.
The Mayo research team, led by
Malcolm A. Leissring, Ph.D.,
neuroscientist at Mayo
Clinic in Florida, made the discovery by testing hundreds of enzymes for
the ability to lower beta-amyloid levels. BACE2 was found to lower beta-amyloid
more effectively than all other enzymes tested. The discovery is
interesting because BACE2 is closely related to another enzyme, known as
BACE1, involved in producing beta-amyloid.
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Alzheimer's, Dementia & Mental Health
"Despite their close similarity, the two enzymes
have completely opposite effects on beta-amyloid — BACE1 giveth, while
BACE2 taketh away," Dr. Leissring says.
Beta-amyloid is a fragment of a larger protein,
known as APP, and is produced by enzymes that cut APP at two places.
BACE1 is the enzyme responsible for making the first cut that generates
beta-amyloid. The research showed that BACE2 cuts beta-amyloid into
smaller pieces, thereby destroying it, instead. Although other enzymes
are known to break down beta-amyloid, BACE2 is particularly efficient at
this function, the study found.
Previous work had shown that BACE2 can also lower
beta-amyloid levels by a second mechanism: by cutting APP at a different
spot from BACE1. BACE2 cuts in the middle of the beta-amyloid portion,
which prevents beta-amyloid production.
"The fact that BACE2 can lower beta-amyloid by two
distinct mechanisms makes this enzyme an especially attractive candidate
for gene therapy to treat Alzheimer's disease," says first author Samer
Abdul-Hay, Ph.D., a neuroscientist at Mayo Clinic in Florida.
The discovery suggests that impairments in BACE2
might increase the risk of
Alzheimer's disease. This
is important because certain drugs in clinical use — for example,
antiviral drugs used to treat human immunodeficiency virus (HIV) — work
by inhibiting enzymes similar to BACE2.
Although BACE2 can lower beta-amyloid by two
distinct mechanisms, only the newly discovered mechanism — beta-amyloid
destruction — is likely relevant to the disease, the researchers note.
This is because the second mechanism, which involves BACE2 cutting APP,
does not occur in the brain. The researchers have obtained a grant from
National Institutes of Health
to study whether blocking beta-amyloid destruction by BACE2 can increase
the risk for Alzheimer's disease in a mouse model of the disease.
The research was supported by a grant from the
Coins for Alzheimer's Research Trust
Fund in affiliation with the
American Federation for Aging
About Mayo Clinic
Mayo Clinic is a nonprofit worldwide leader in
medical care, research and education for people from all walks of life.
For more information, visit
Mayo Clinic in Florida
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