beta-amiloid peptid okozta intracelluláris kalciumszint-változások Alzheimer-kórban szenvedó betegek fibroblastjain.

András Palotás, János Kálmán, Gábor Laskay, Anna Juhász, Zoltán Janka, Botond Penke

Research output: Article

Abstract

RATIONALE: beta-amyloid peptides, comprising the major neuropathological lesions of Alzheimer's disease, have been found to form depositions in various peripheral tissues, including the skin. Neurons in the disorder succumb to the altered ionic homeostasis and some other factors caused by this toxic peptide. In line with these findings, our study aimed to find differences in biochemical processes of cultured cutaneous fibroblasts derived from sporadic Alzheimer patients and from age-matched control individuals that may mirror changes in the central nervous system. METHODS: Intracellular ionic homeostasis of Alzheimer and control fibroblasts was measured in Fura-2AM-loaded human fibroblasts by dual wavelength spectrofluorimetry. RESULTS: Cells derived from Alzheimer patients exhibited lower intracellular free calcium levels as compared to the control cultures. Exposure of fibroblasts to beta-amyloid resulted in increased calcium concentrations of the control cells, but not of Alzheimer ones. CONCLUSION: Our findings indicate that Alzheimer's disease is a systemic disorder that, among others, affects the calcium homeostasis of fibroblasts. Even though it is unknown whether the diminished ionic response of Alzheimer fibroblasts is a disease or actual status marker, it could prove to be a useful model for the analysis of Alzheimer specific changes.

Original languageHungarian
Pages (from-to)164-167
Number of pages4
JournalIdeggyógyászati szemle
Volume55
Issue number5-6
Publication statusPublished - máj. 20 2002

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ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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