Testosterone may prevent Alzheimer's disease

Orli Belman:

Researchers at the University of Southern California have discovered a direct link between loss of testosterone and the development of an Alzheimer's-like disease in mice. They also discovered that testosterone treatment slows progression of the disease.

The study, published in the December 20 issue of The Journal of Neuroscience, predicts that testosterone-based hormone therapy may be useful in the treatment and prevention of Alzheimer's disease in aging men.

"We've known that low testosterone is a risk factor for Alzheimer's disease but now we know why," said Christian Pike, senior author and associate professor at the Leonard Davis School of Gerontology at USC. "The implication for humans is that testosterone therapy might one day be able to block the development of the disease."

In order to investigate testosterone's role in the development of Alzheimer's disease, the team took away the ability of male mice to produce testosterone. Some mice were then given a form of testosterone while others were given none.

The mice with lowered testosterone showed increases in levels of the protein beta-amyloid, which has been widely implicated as playing a role in the development of Alzheimer's disease. They also showed signs of behavioral impairment.

The mice that were given testosterone showed reduced accumulation of beta-amyloid and less behavioral impairment.

"These results are exciting because they tell us that we are on to something that is worth pursuing," said Pike. "The next step is to look at what the long term effects of testosterone therapy are in aging men."

This study adds valuable new information to understanding the role of hormones in aging and disease. Recent evidence has suggested that testosterone may be useful in other neurological conditions. In a presentation at the Society of Neuroscience's annual meeting this fall, Chien-Ping Ko, professor of biological sciences at USC reported that testosterone therapy improved muscle coordination in mice suffering from a form of Amyotrophic Lateral Sclerosis, Lou Gehrigs Disease.

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