New implications of memory mechanisms for Alzheimer's disease.

R. Etcheberrigaray; E. Ito; K. Oka; B. Tofel-Grehl; G. E. Gibson; D. L. Alkon

New implications of memory mechanisms for Alzheimer's disease.

R. Etcheberrigaray, E. Ito, K. Oka, B. Tofel-Grehl, G. E. Gibson, D. L. Alkon

研究成果: Article › 査読

抄録

Previous studies of molluscan and mammalian neural networks have implicated potassium channels, calcium-dependent kinases and a small G-protein (Cp20) in associative memory storage. Since Alzheimer's disease is characterized by memory deficits and possible changes in PKC activation, we studied potassium channel function in AD. Patch-clamp experiments revealed the absence of a 113 pS TEA-sensitive K⁺ channel in fibroblasts from Alzheimer's but not control patients. These results suggest a role for potassium channel dysfunction in Alzheimer's disease.

本文言語	English
ページ（範囲）	S7-S10
ジャーナル	Neuroscience Research Communications
巻	12
号	SUPPL. 1
出版ステータス	Published - 1993
外部発表	はい

ASJC Scopus subject areas

神経科学（全般）

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AU - Ito, E.

AU - Oka, K.

AU - Tofel-Grehl, B.

AU - Gibson, G. E.

AU - Alkon, D. L.

PY - 1993

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AB - Previous studies of molluscan and mammalian neural networks have implicated potassium channels, calcium-dependent kinases and a small G-protein (Cp20) in associative memory storage. Since Alzheimer's disease is characterized by memory deficits and possible changes in PKC activation, we studied potassium channel function in AD. Patch-clamp experiments revealed the absence of a 113 pS TEA-sensitive K+ channel in fibroblasts from Alzheimer's but not control patients. These results suggest a role for potassium channel dysfunction in Alzheimer's disease.

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KW - Memory

KW - Potassium channels

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ER -

New implications of memory mechanisms for Alzheimer's disease.

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