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PET scans of a normal brain (left) and
Alzheimer's brain (right).
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Alzheimer's Disease is a tragic illness.
A degenerative brain disease that affects one in 10 people over 65,
it causes sufferers to become confused and lose their cognitive
functions, undoing them mentally and physically with a terrifying
relentlessness, scrolling their hard-won adult competencies back to
helpless inability to care for themselves, causing them to forget
the very faces and names of their loved ones and the memories that
help make them who they are. The course of the disease may take
years, but it ends in death.
Though Alzheimer's is a disease
and not a natural result of aging, the risk does increase with age
-- nearly half of everyone over 85 has Alzheimer's disease. Because
the population is aging, the number of Alzheimer's patients in the
U.S. is expected to rocket from 4 million now to 14 million by the
year 2050. According to some estimates, the annual total cost of
caring for Alzheimer's patients in the U.S. is already as much as
$100 billion; not to mention the huge cost in human suffering for
both patients and caregivers.
Finding a treatment for or,
better still, a way to prevent Alzheimer's would clearly be a
tremendous medical, social and humanitarian boon. So far, there is
no medical treatment available to cure or halt Alzheimer's, though
drugs exist that may temporarily relieve some symptoms.
But
it is a tremendously exciting time in Alzheimer's research. Hundreds
of promising discoveries have been made in the past few years, and
at least one group of researchers may be on the brink of a finding a
viable treatment, or at least a greatly improved understanding of
what causes the disease.
Efforts to find a way to prevent or
treat Alzheimer's are proceeding along many different avenues. Here
are some of the areas considered most promising:
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On the neural level, a healthy
neuron (top) and a neuron with the plaques and tangles of
Alzheimer's (bottom).
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When researchers earlier in this century
dissected the brains of deceased Alzheimer's patients, they noticed
that the brains were full of two kinds of obviously abnormal
structures: what are now referred to as plaques and tangles. Plaques
are abnormal build-ups, in the spaces between the afflicted brain's
nerve cells, of a kind of protein fragment called beta-amyloid.
Tangles are abnormal collections, inside neurons, of twisted threads
made up of a protein called tau.
For a long time,
researchers have struggled to understand whether plaques and tangles
are causes or results of Alzheimer's disease, and which of the two
is the more significant pathology. Much of the current research is
taking the tack that plaque formation is the more significant, and a
central process in the disease's terrible progression.
In an
exciting development, the Irish drug company Elan and Wyeth-Ayerst
Laboratories in New Jersey, working jointly, announced in July 2001
that they are about to begin human testing of a new Alzheimer's
"vaccine" that could halt or even cure the disease. The "vaccine,"
called AN-1792, contains bits of beta-amyloid. When injected into a
person's arm, it will -- its developers hope -- stimulate the body's
antibodies to seek out and remove the foreign intruder,
beta-amyloid, just as a flu vaccination stimulates the body's
antibodies to the flu virus. This immune response, hopefully, will
clean out the beta-amyloids forming plaques in the brain.
The vaccine has been shown to be somewhat successful in mice
and safe in humans. The new human tests, set to begin in the fall of
2001, should show whether it works to treat people with Alzheimer's.
"Everybody is excited about AN-1792," said Bill Thies, vice
president of medical and scientific affairs for the Alzheimer's
Association. "It is going to be the first test of a critical theory
about Alzheimer's disease -- whether lowering levels of amyloids
halts the progression of the disease. Even if it fails, you'll have
a very important piece of information about the disease causes and
process." Meanwhile, other teams of researchers are looking for ways
to block or prevent the production of amyloids in the brain in the
first place.

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