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In the News
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Body & Brain Apnea-dementia link
Antidepressants
show signs
of countering
Alzheimer’s
Mouse and human data link
drugs to less plaque in brain
STORY ONE
By Laura Sanders
Widely used antidepres- sants may reduce the ominous brain plaques associatedwith Alzheimer’s disease, a new study in mice and
humans finds.
Brain scans of people who have taken
antidepressants reveal fewer clumps
of the protein amyloid-beta, a target of
Alzheimer’s prevention strategies, compared with people who have not taken
the drugs.
Many in the field have voiced caution about the results. But if borne out
by further study, the findings may point
to a new, relatively safe way to treat and
prevent Alzheimer’s disease, which is
the sixth leading cause of death in the
United States.
“I think this is a wonderful piece of
news, and I think there’s going to be a lot
of excitement about this,” says internist
Michael Weiner, who leads the Alzheimer’s Disease Neuroimaging Initiative at
the Veterans Affairs Medical Center
campus of the University of California, San Francisco. “It points the way
towards a possible approach to treating
Alzheimer’s disease that people have not
After taking an antidepressant for four months, mice had less amyloid-beta plaque
(brown clumps, left) in their brains than mice that didn’t take the drug (right).
been talking about very much.”
In the study, mice genetically engi-
neered to overproduce amyloid-beta,
or A-beta, were given one of three selec-
tive serotonin reuptake inhibitors, a
class of antidepressants that boost cir-
culating levels of the chemical messen-
ger serotonin in the brain. After a single
dose of the antidepressants, A-beta lev-
els dropped in the fluid that surrounds
mouse brain cells, researchers report
online August 22 in the Proceedings of
the National Academy of Sciences. A full
day after receiving the drug, the mice’s
A-beta levels fell by nearly a quarter.
Long-term administration of the drug
had a larger effect. Engineered mice that
took the SSRI citalopram for four months
had about half the A-beta plaques in their
brains as mice that hadn’t received the
drug. This reduction seems to happen
through a protein called ERK, which
serves as the middleman between brain
cells’ serotonin-sensing proteins and
A-beta production.
Figuring out the details of this process may open the door for developing
new ways to prevent A-beta buildup,
says study coauthor John Cirrito of the
Washington University School of Medicine in St. Louis.
To see if a similar effect might be
happening in people, the scientists
scanned the brains of 186 cognitively
normal elderly people and looked for
signs of A-beta plaques. The team used
a compound called PIB that binds to big
clumps of A-beta in the brain and glows
on a PET scan.
Of these participants, 52 reported that
they had taken an antidepressant in the
last five years. These people, researchers found, had about half the A-beta load
in their brains as the people who hadn’t
taken an antidepressant. What’s more,
the length of time the participants took
the drugs correlated with the density of
A-beta plaques in the brain — the longer
the antidepressant use, the less plaque.
“We think there are influences
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September 10, 2011 | SCIENCE NEWS | 5
