Alzheimer’s disease appears to have multiple causes,
and scientists are slowly unraveling them
By Alice Dembner
GLOBE STAFF
A century after Alois Alzheimer identified the
debilitating dementia that carries his name, scientists
are still trying to determine what causes the
disease in old age. Their quest takes on increasing
urgency, with predictions that unless a cure is found,
the number of Americans with the disease will rise
from about 4.5 million now to 13 million in 2050.
Many scientists believe that Alzheimer’s results
from a complex interplay of environmental factors,
lifestyle choices, and genes and proteins gone haywire.
But the changes in the brain that characterize
the disease develop over decades and also occur in
some healthy seniors, making it diffi cult to sort out
the culprits from the bystanders.
Yet, tantalizing tidbits have surfaced in the last
few weeks, including discovery of a new genetic
mutation that appears to increase the risk of getting
Alzheimer’s and new evidence that insulin defi ciencies
may contribute to deterioration of the brain.
“The pieces are coming together. We’ve got the
outline of the puzzle in place, and we’re beginning to
see the form,” said Stephen Snyder, who oversees
research on the causes of Alzheimer’s for the National
Institute on Aging. “It’s probably fi ve or six genes and
a dozen proteins that get out of kilter,” said Snyder, and certainly not just the sticky clumps of
proteins called beta-amyloid plaques that
have received the most attention.
In the brain, the disease’s hallmarks
are those plaques, tangles of another protein
called tau, and the progressive death
of nerve cells, called neurons, that gradually
strip a victim of memory, language,
reasoning, and, finally, life.
Mutations in three genes cause earlyonset
Alzheimer’s, the rare form of the
disease that strikes people in their 30s,
40s, or 50s. Those altered genes trigger
production of too much beta-amyloid. But
none appears to be involved in the kind of
Alzheimer’s that strikes after age 60.
So far, researchers have linked two major
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and are on the trail of four or five more.
These mutations do not cause the disease,
but rather increase the risk of developing
it. One, ApoE4, increases the risk of getting
the disease three- to four-fold. A second
potential gene mutation, called
UBQLN-1, was identified this month by
Rudy Tanzi, a geneticist at Massachusetts
General Hospital. Tanzi, founder of TorreyPines
Therapeutics, which is working
on Alzheimer’s drugs, said he believes it
may increase the risk one- to two-fold, but
its specific role in the disease has not been
determined.
The lead suspect in the search for a
cause remains the protein beta-amyloid
because of its clear involvement in early
onset Alzheimer’s and its big presence in
Alzheimer’s brains.
Tests of an amyloid vaccine in people,
which might have proved amyloid’s leading
role, were halted in 2002 when 18 of
300 subjects developed a potentially fatal
brain inflammation. Nevertheless, some
participants showed inklings of a positive
effect, enough to keep researchers pursuing
similar experiments. In addition, antibodies
to amyloid reversed memory problems
in mice, and cleared out amyloid
deposits and then tau.
‘‘It’s my feeling that all the cases of Alzheimer’s
are caused by an imbalance in
the accumulation versus removal of the
beta-amyloid protein,’’ said Dr. Dennis
Selkoe, a leading amyloid researcher who
is codirector of the Center for Neurologic
Diseases at Brigham and Women’s Hospital,
and who is a director of Elan Corp.,
which is working on amyloid-based treatments.
Much of the amyloid research is shifting