Protein Found that Prevents Key Alzheimer's Pathology
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A better understanding of the insidious forces that culminate in Alzheimer's disease was revealed here today.
The process of protein slicing that leads to the development and accumulation of beta-amyloid plaques in the brains of Alzheimer's patients appears to cut both ways, reported Peter St. George-Hyslop, M.D., D.Sc., director of the Center for Research in Neurodegenerative Disease at the University of Toronto, and colleagues, in the April 27 issue of Nature.
A lowly "cargo transporter" protein called TMP21 seems to play a key role in preventing the abnormal cleavage of amyloid precursor protein (APP) into beta-amyloid fragments, they found. At the same time, TMP21 does not interfere with a different form of protein cleavage essential for normal cell signaling processes, they said.
The discovery could lead the way to new therapies for preventing or treating Alzheimer's, perhaps an analog of TMP21 that targets the abnormal cleavage while leaving other protein slicing functions intact.

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