Strategy Could Put Brakes on Alzheimer's

THURSDAY, May 3 (HealthDay News) -- By cutting levels of a brain protein called "tau," scientists were able to preserve the memory and lifespans of mice genetically engineered to develop Alzheimer's disease.

The finding, while early, could point to effective strategies to protect aging humans against the brain-robbing illness.

"We found a way to make brain cells in the brain more resistant to poisonous amyloid protein that builds up in the brain," explained study senior author Dr. Lennart Mucke, director of the Gladstone Institute of Neurological Disease and professor of neurology at the University of California, San Francisco.

"The trick we used was to reduce normal [tau] protein that we all make by half," Mucke said. This strategy "somehow made the cells of the brain and memory resistant to the detrimental effects of amyloid protein," he explained

One expert was impressed by the findings. "This provides scientists with a new target, or rather, re-tools a known substance into a potential drug target," said Dr. Sam Gandy, chair of the Medical and Scientific Advisory Council of the Alzheimer's Association, and director of the Farber Institute for Neurosciences at Thomas Jefferson University, Philadelphia.

The findings, reported in the May 4 issue ofScience, would be a complement to current efforts to combat Alzheimer's by reducing levels of amyloid protein in the brain.

There are currently no effective treatments for Alzheimer's disease, which now affects over 5 million Americans, according to the Alzheimer's Association. Scientists now project that unless new ways are found to prevent or treat the disease, the total could climb to 16 million by mid-century.

Much current research focuses on reducing the buildup in the brain of clumps of amyloid-beta protein, which are believed to cause the disease. This strategy would complement that approach.

"I'm very enthusiastic about anti-amyloid treatment but I thought it would be very useful to have a complementary approach to make the brain more resistant to whatever amyloids you can't get rid of," Mucke explained.

In a normal brain, "tau acts to form part of the scaffolding or skeleton that gives the nerve cell its shape," Gandy said. In an Alzheimer's brain, however, the scaffolding collapses and forms "neurofibrillary tangles."

"Conventional wisdom would've predicted that tau deficiency would be a very bad thing -- and that may still be true for severe deficiencies -- but the good news is that dialing down the tau level just a small bit may be sufficient to cause this newly observed benefit," Gandy said.

In this experiment, Mucke and his team eliminated one or both copies of the tau gene in mice genetically engineered to produce amyloid proteins.