Study shows hormone replacement may cut dementia risk
Sharon Kirkey , CanWest News Service
Testosterone patches can not only boost potency and sex drive, they may protect the male brain from Alzheimer’s disease.
A new study shows testosterone therapy reduces levels of a sticky protein that causes plaque buildup in the brains of people with Alzheimer’s.
So far, the work has been done only in mice. But University of Southern California researchers believe “that we are on to something” and that testosterone replacement therapy might one day treat or prevent Alzheimer’s in aging men.
“We’ve known that low testosterone is a risk factor for Alzheimer’s disease, but now we know why,” senior author Christian Pike, an associate professor at the Leonard Davis School of Gerontology, said in statement released with the study. “The implication for humans is that testosterone therapy might one day be able to block the development of the disease.”
An estimated 290,000 Canadians over 65 have Alzheimer’s, a number expected to double over the next two decades.
Like grey hair and wrinkles, all men experience a drop in their testosterone levels as a normal consequence of growing old.
Recent studies have shown that men with low testosterone seem to be at an increased risk of Alzheimer’s, but no one knew why.
Today’s study, published in The Journal of Neuroscience, provides the first experimental data linking testosterone depletion to Alzheimer’s-like changes in the brain.
Mice don’t normally get Alzheimer’s disease, so the California team used genetically engineered rodents that carry three different human genes tied to neurodegenerative disease. The mice all developed a form of Alzheimer’s.
When the team took away the ability of male mice to make testosterone, the rodents developed Alzheimer’s disease much faster. They had more of a protein called beta-amyloid which, if produced in excess, clumps together into plaques, killing neurons.
“What that suggests to us, if you dare to extrapolate to the human condition, is that low testosterone might be creating in the human brain an environment where Alzheimer’s disease can really progress rapidly,” Pike said.
The low-testosterone mice also performed poorly in a Y maze task that involves the hippocampus, a region of the brain critical for memory and one of the first areas attacked in humans with Alzheimer’s.
Some of the mice were put on testosterone therapy. Three months later, they had less beta-amyloid and less behavioural impairment than untreated mice.
“These results are exciting because they tell us that we are on to something that is worth pursuing,” Pike said.
He cautioned that it’s premature to recommend men jump on testosterone therapy.
“Given what happened with post-menopausal women jumping on estrogen-based hormonal therapies — we had the promise of Alzheimer’s protection, we had the promise of protection against osteoporosis . . . .
“There potentially might be the same sorts of problems with men.”
Testosterone has been implicated in prostate cancer.