Alzheimer and β-amyloid-treated fibroblasts demonstrate a decrease in a memory-associated GTP-binding protein, Cp20

Christopher S. Kim, Yifan Han, René Etcheberrigaray, Thomas J. Nelson, James L. Olds, Tohru Yoshioka, Daniel L. Alkon

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The two proteins most consistently identified in the brains of patients with Alzheimer disease (AD) have been β-amyloid and tau, whose roles in the physiology or pathophysiology of brain cells are not fully understood. To identify other protein(s) involved in AD that have been implicated in physiological contexts, we undertook to analyze a specific memory-associated protein, Cp20, in fibroblasts from AD and control donors. Cp20, a GTP- binding protein that is a member of the ADP-ribosylation factor family, was significantly decreased in fibroblasts from AD patients. Normal control fibroblasts exposed to 10 nM β-amyloid, the same concentration that induced AD-like K+changes in control fibroblasts, showed a similar decrease in Cp20. Since it has been previously demonstrated that Cp20 is a potent regulator of K+channels, these findings suggest that changes in this memory-associated protein may explain previously observed differences in AD K+channels and suggest a pathophysiologic involvement linked to soluble β- amyloid metabolism that could contribute to the characteristic memory loss of AD.
Original languageEnglish
Pages (from-to)3060-3064
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number7
Publication statusPublished - 28 Mar 1995
Externally publishedYes

ASJC Scopus subject areas

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