Pro-apoptotic effects of tau mutations in chromosome 17 frontotemporal dementia and parkinsonism

Katsutoshi Furukawa, Ian D'Souza, Christopher H. Crudder, Hiroshi Onodera, Yasuto Itoyama, Parvoneh Poorkaj, Thomas D. Bird, Gerard D. Schellenberg

Research output: Contribution to journalArticlepeer-review

23 Citations (Scopus)

Abstract

It was recently discovered that mutations of tau cause hereditary frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17). Here we report that cultured SH-SY5Y human neuroblastoma cells transfected with mutated tau genes are more vulnerable to apoptotic stimulus. Two kinds of mutations of tau causing FTDP-17 were examined in the present study: one was in exon 10 (N279K) and the other was in exon 12 (V337M). SH-SY5Y cells transfected with either mutated tau were more vulnerable to serum withdrawal, whereas cells transfected with the wild-type tau or vector alone showed no significant change in apoptotic vulnerability. The increase in the intracellular calcium concentration by the serum withdrawal was significantly greater in the SH-SY5Y cells transfected with mutated tau genes than in cells transfected with the wild-type tau or vector alone. These results suggest that mutations of tau might cause FTDP-17 by these pro-apoptotic functions by disrupting the intracellular calcium homeostasis.

Original languageEnglish
Pages (from-to)57-60
Number of pages4
JournalNeuroReport
Volume11
Issue number1
Publication statusPublished - 2000 Jan 17

Keywords

  • Apoptosis
  • Calcium
  • Frontotemporal dementia and parkinsonism
  • Mutation
  • Tau

ASJC Scopus subject areas

  • Neuroscience(all)

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