In Mice, Brain Cells Discovered That Might Control Aging
by -- Robert Preidt
Updated: Jul 26th 2017
WEDNESDAY, July 26, 2017 (HealthDay News) -- Scientists working with mice believe they've identified brain cells that control aging.
The discovery could lead to new ways to treat age-related diseases in people and extend lives, according to researchers at the Albert Einstein College of Medicine in New York City.
Their laboratory experiments suggest that adult neural stem cells in the brain's hypothalamus regulate the speed of aging in the body.
The hypothalamus plays a role in important processes, such as growth, development, reproduction and metabolism. It was already known that the adult neural stem cells identified in this study are responsible for forming new brain neurons -- cells.
"Our research shows that the number of hypothalamic neural stem cells naturally declines over the life of the animal, and this decline accelerates aging," said study senior author Dr. Dongsheng Cai.
"But we also found that the effects of this loss are not irreversible," said Cai, a professor of molecular pharmacology.
"By replenishing these stem cells or the molecules they produce, it's possible to slow and even reverse various aspects of aging throughout the body," he said in a college news release.
The researchers found that the number of hypothalamic stem cells in mice began to diminish when they were about 10 months old, several months before the usual signs of aging start appearing.
"By old age -- about 2 years of age in mice -- most of those cells were gone," Cai said.
The next step is to determine how these stem cells control aging. That could eventually lead to new ways to treat age-related diseases and slow the aging process in people, the study authors suggested.
However, while these early results appear promising, results of animal experiments often aren't replicated in humans.
The study was published online July 26 in the journal Nature.
The U.S. Centers for Disease Control and Prevention offers resources on healthy aging.
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