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Potassium channel dysfunction in fibroblasts identifies patients with Alzheimer disease.

1993; National Academy of Sciences; Volume: 90; Issue: 17 Linguagem: Inglês

10.1073/pnas.90.17.8209

1091-6490

René Etcheberrigaray, Etsuro Ito, Kotaro Oka, B. Tofel-Grehl, Gary E. Gibson, D L Alkon,

Ion channel regulation and function

Since memory loss is characteristic of Alzheimer disease (AD), and since K+ channels change during acquisition of memory in both molluscs and mammals, we investigated K+ channel function as a possible site of AD pathology and, therefore, as a possible diagnostic index as well. A 113-pS tetraethylammonium (TEA)-sensitive K+ channel was consistently absent from AD fibroblasts, while it was often present in young and aged control fibroblasts. A second (166-pS) K+ channel was present in all three groups. Elevated external potassium raised intracellular Ca2+ in all cases. TEA depolarized and caused intracellular Ca2+ elevation in young and aged control fibroblasts but not AD fibroblasts. The invariable absence of a 113-pS TEA-sensitive K+ channel and TEA-induced Ca2+ signal indicate K+ channel dysfunction in AD fibroblasts. These results suggest the possibility of a laboratory method that would diagnostically distinguish AD patients, with or without a family history of AD, from normal age-matched controls and also from patients with non-AD neurological and psychiatric disorders.