Fewer calories may slow Alzheimer’s

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.

From USC:

Fewer calories may slow Alzheimer’s

A restrictive diet in mice reduces the build-up of a substance linked to memory loss. But can the findngs be applied to humans?

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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