Key Role Found for Tau Protein in Alzheimer's

Experiments have revealed evidence that tau protein must be present to enable beta-amyloid to induce the degeneration of brain cells that occurs in Alzheimer's disease. The finding was reported in the April 30, 2002, issue of the Proceedings of the National Academy of Science.

Previous investigations have not been able to determine whether neurofibrillary tau tangles or beta-amyloid plaques are the primary cause of Alzheimer's disease or to find a link between the two. Both are often found in the same brain regions of people with Alzheimer's disease. Now, researchers from Northwestern University Institute for Neuroscience (NUIN, Chicago, IL, USA) have found a definite connection between the two. Their experiments showed that neurons with normal amounts of tau degenerated in the presence of beta-amyloid, while neurons treated to have no tau did not degenerate.

An analysis of the composition of the cytoskeleton of tau-depleted neurons revealed rapid turnover of microtubules, which stabilize the cell's shape and serve as a kind of molecular transport system. This suggests that if neurons can maintain the composition of microtubules with rapid turnover as they age, they may be resistant to neurodegeneration.

"These findings identify the dynamic behavior of the microtubules as a new target for therapeutic intervention,” said Adriana Ferreira, M.D., assistant professor of cell and molecular biology and NUIN researcher. "They also suggest that factors able to induce or restore a more plastic composition of the microtubules might prevent the neuronal degeneration associated with the formation of senile plaques in Alzheimer's disease patients.”




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