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2004 News Archives
Fewer Calories Could Slow Alzheimer’s
12/14/04
A USC study with mice finds that a restrictive diet reduces
build-up of a substance linked to memory loss. The research raises
questions about whether the findings can be applied to humans.
By Usha Sutliff
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| “This is the first indication that modest
changes in the normal diet can slow some aspects of Alzheimer’s
disease,” said Finch, co-author of the study published
in the online version of the journal Neurobiology of Aging. |
Restricting the diets of mice reduces the build-up of plaques
in the brain that are linked to Alzheimer’s disease, according
to a USC study.
With obese people generally considered to be at a higher risk for
developing Alzheimer’s, the research raises questions about
whether the findings are potentially applicable to humans.
“This is the first indication that modest changes in the
normal diet can slow some aspects of Alzheimer’s disease,”
said Caleb Finch, co-author of the study published in the online
version of the journal Neurobiology of Aging.
“But that is far and away yet to be proven for humans. It’s
a big jump to say that what’s true for a mouse in a cage is
relevant to people living in our complex world,” Finch said.
In the study, conducted with collaborators at the University of
South Florida in Tampa, researchers used mice whose DNA had been
altered with human genes from two families with early onset hereditary
Alzheimer’s.
The mice were then split into two groups as young adults: one that
could eat all it desired (“ad libitum”) and the other
that had its food intake reduced by 40 percent over a four-week
period (diet-restricted).
The researchers were looking specifically at the formation of plaques
caused by a build-up of the fiber-like substance called beta-amyloid.
Made up of proteins and polysaccharides, amyloid plaques are deposited
in the brain during Alzheimer’s disease. Specifically, plaques
accumulate in the hippocampus and frontal cortex of Alzheimer’s
sufferers – areas responsible for memory.
In the diet-restricted mice, both the amount and size of plaque
was about 50 percent less than in mice that ate as much as they
wanted.
“The power of this study is that two different sets of [human]
family mutations were equally sensitive to the effect of diet and
slowing the Alzheimer’s-like change,” said Finch, holder
of the ARCO-William F. Kieschnick Chair in the Neurobiology of Aging
at USC.
The next goal is to find out why diet restriction has such profound
and rapid effects, Finch said.
“We are going to look into the details of metabolism to try
and isolate which of the consequences of diet restriction is at
work,” Finch said. “Is it the blood glucose? Is it the
lowered insulin? Those are two targets.”
The other USC researchers on this study were Nilay V. Patel, a
former USC postdoc who is now a staff scientist at City of Hope
Medical Center, and Todd E. Morgan, a research assistant professor
in the Andrus Gerontology Center at USC.
The researchers at the University of Southern Florida are Marcia
Gordon, Karen E. Connor, Robert A. Good, Robert W. Engelman, Jerimiah
Mason and David G. Morgan.
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