Your Health ;
; Scientists once thought plaques were bad.
; New studies show they may protect the brain.
; Some researchers see a new villain.
By Elizabeth Agnvall
players in the rogue process that attacks the brain.
“Plaques are no longer where the action is,” says Sam
Gandy, M.D., of the Alzheimer’s Disease Research Cen-
ter at Mount Sinai School of Medicine in New York.
Gandy’s work builds on several years of research that
has been moving toward this new theory. And if the the-
ory is correct, then drugs that target plaques—as many
of the most promising medications have done in the past
few years—may not help people who have the disease.
They could even make them worse. This research is key.
About 5.1 million Americans have Alzheimer’s, and that
number will grow as boomers age.
Gandy’s work with specially engineered mice—which
developed Alzheimer’s though they had only clumps of
the oligomers and no plaques in their brains—“is the
final experiment that’s making the whole field turn
around,” says Andrew Dillin, a scientist who studies
aging and the brain at the Salk Institute of California.
The role amyloid beta plays in the development of the
disease was a hot topic at the international Alzheimer’s
conference in Hawaii this summer.
While the development is exciting, William Thies,
the Alzheimer’s Association’s chief medical officer,
New research appears to upend our current understanding of the causes of Alzheimer’s
disease, and may lead to a whole new approach to
finding a cure for the devastating dementia.
The controversial new theory gaining traction in the
scientific community is that in Alzheimer’s disease the
brain is destroyed not by sticky plaques—long held to be
the culprit—but by free-floating clumps of protein.
In fact, the sticky plaques that surround the brain cells
of those with Alzheimer’s may be the body’s way of pro-
tecting against these toxic clumps.
For the last 20 years, following the prevailing theory
that sticky plaques cause Alzheimer’s disease, drug
developers have been targeting those plaques in their
search for a cure.
But recently published studies on mice and rats may
prove to be the tipping point that takes research in a
new direction. Many scientists now believe clumps
of amyloid beta protein called oligomers are the main
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