Alzheimer’s mystery protein unmasked

A protein that forms plaques in people with Alzheimer’s disease takes part in the normal process of forgetting and remembering, a new study suggests.

Scientists have long wondered why neurons make beta-amyloid, also called A-beta. This sticky protein forms the characteristic, neuron-smothering plaques of Alzheimer’s disease. A-beta forms when enzymes snip a large protein called amyloid precursor protein (APP) into smaller pieces. A-beta then sticks to intact APPs, stimulating enzymes called caspases to clip APPs again.

A new study of human brain tissue suggests that the process is needed for deleting unnecessary memories to clear space on the brain’s hard drive for new information.

Brains of Alzheimer’s patients had four times more caspase cleavage of APP than brains of healthy older people, says Dale Bredesen of the Buck Institute for Age Research in Novato, Calif. But he and his colleagues were surprised to find that healthy young people had 10 times more cleavage than people with Alzheimer’s disease.

Bredesen suggests that young brains make and dissolve memories at Ferrari speeds, but older brains gradually get slower at both remembering and forgetting. People with Alzheimer’s “get stuck in reverse,” dissolving memories faster than they make them, Bredesen says.

The research appeared in the March 7 issue of the Journal of Alzheimer’s Disease.

Tina Hesman Saey

Tina Hesman Saey is the senior staff writer and reports on molecular biology. She has a Ph.D. in molecular genetics from Washington University in St. Louis and a master’s degree in science journalism from Boston University.

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