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Can Mental Function be Restored in Alzheimer's Disease?

Mouse experiment raises hope of healing brain cells

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HealthDay Reporter

THURSDAY, July 14, 2005 (HealthDay News) -- An animal experiment raises the hope of future treatment that might restore at least a portion of mental function lost to Alzheimer's disease.

Mice genetically engineered to suffer Alzheimer's-like memory loss regained some of that memory when the disabling gene was turned off, according to a report in the July 15 issue of Science by researchers at the University of Minnesota.

The restoration of lost cognitive function is a revolutionary idea, the researchers say, because so far studies have centered on slowing the loss of mental function in Alzheimer's patients, not reversing it.

The mice in the experiment suffered a major loss of neurons, the brain cells that drive thinking. That loss was not restored, said study author Dr. Karen Ashe, a professor of neurology. However, she said the mice's memory ability nevertheless improved.

"That implies that the remaining neurons were functioning improperly," Ashe said. "If we discover a way to remove the molecules affecting the remaining neurons, Alzheimer's patients who have lost neurons would regain their ability to learn," she speculated.

Ashe pointed to one molecule as a prime suspect -- some abnormal form of tau, a protein that plays a key role in structuring the brain.

The villainous tau molecule is not the one found in the fibrous tangles that are one of the two visible features of Alzheimer's disease, Ashe added. Mice recovered their memory even though the number of tangles in their brains increased, she pointed out.

"These neurofibrillary tangles -- one of the defining features of Alzheimer's disease -- are not the cause of the memory problems," she said.

Therapy aimed at the other major feature of the disease, toxic deposits of a protein called beta-amyloid, is just now moving into the clinic, said William Thies, vice president for medical and scientific affairs at the Alzheimer's Association. That therapy developed from animal experiments similar to the one reported by Ashe and her colleagues, he noted.

Her team "have produced a tool with which people can begin to explore whether limiting tau can be a good endpoint," Thies said.

Mice in the study were trained to swim to a submerged platform in a pool of water. They lost the ability to find the platform when the damaging gene was in action and regained it when the gene was turned off -- a surprising gain in memory.

"Many of us have thought that the brains of Alzheimer's patients have live neurons, dead ones and sick ones," Thies said. "If you remove whatever is irritating the sick ones, they can get better."

While the new study centered on tau, "maybe the ultimate treatment is something that reduces the accumulation of both amyloid and tau," Thies said.

The form of tau that may become a target for treatment is unknown, Ashe said. "Maybe there are other abnormal forms of tau that have not been found," she said. "After all, these are not even visible under the microscope."

And the same can be true of amyloid, Ashe said. "The important message here is that we need to known which forms of beta-amyloid and which forms of tau we want to target," she said.

More information

Find out more about advances in Alzheimer's research at the Alzheimer's Association.

SOURCES: Karen Ashe, M.D., Ph.D, professor, neurology, University of Minnesota, Minneapolis; William Thies, Ph.D., vice president, medical and scientific affairs, Alzheimer's Association, Chicago; July 15, 2005, Science

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