ArticleProceedings of the National Academy of Sciences of the United States of America1995
Alzheimer and beta-amyloid-treated fibroblasts demonstrate a decrease in a memory-associated GTP-binding protein, Cp20.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 27 citations in OpenAlex.
- Broad DNA repair responses in neural injury are associated with activation of the IL-6 pathway in cholesterol-fed rabbits.Journal of neurochemistry · 2009Article
- Mechanisms of amyloid beta protein-induced modification in ion transport systems: implications for neurodegenerative diseases.Cellular and molecular neurobiology · 2001Review
- Functional switching of GABAergic synapses by ryanodine receptor activation.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- Alzheimer's-specific effects of soluble beta-amyloid on protein kinase C-alpha and -gamma degradation in human fibroblasts.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- Bradykinin-induced amyloid precursor protein secretion: a protein kinase C-independent mechanism that is not altered in fibroblasts from patients with sporadic Alzheimer's disease.The Biochemical journal · 1998Article
- Age-related alteration of PKC, a key enzyme in memory processes: physiological and pathological examples.Molecular neurobiology · 1998Review
- Calexcitin: a signaling protein that binds calcium and GTP, inhibits potassium channels, and enhances membrane excitability.Proceedings of the National Academy of Sciences of the United States of America · 1996Article
- Amyloid beta-protein reduces acetylcholine synthesis in a cell line derived from cholinergic neurons of the basal forebrain.Proceedings of the National Academy of Sciences of the United States of America · 1996Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
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Abstract
The two proteins most consistently identified in the brains of patients with Alzheimer disease (AD) have been beta-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 beta-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 beta-amyloid metabolism that could contribute to the characteristic memory loss of AD.
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