Differential regulation of adenylyl cyclase in fibroblasts from sporadic and familial Alzheimer's disease cases with PS1 and APP mutations

Monika Vestling, Abdu Adem, Marco Racchi, Gary E. Gibson, Lars Lannfelt, Richard F. Cowburn

Research output: Contribution to journalArticlepeer-review

12 Citations (Scopus)

Abstract

β-ADRENOCEPTOR- and forskolin-stimulated adenylyl cyclase activities were determined in primary skin fibroblasts established from patients with sporadic Alzheimer's disease (AD) and from individuals with familial APP KM670/671NL PS1 M146V and PS1 H163Y mutations. Our data showed a significantly decreased β-adrenoceptor-stimulated adenylyl cyclase activity in fibroblasts from sporadic AD compared with age-matched controls (p < 0.001, Student's unpaired t-test). In contrast, both β-adrenoceptor- and forskolin-stimulated adenylyl cyclase activities were significantly increased in fibroblasts bearing PS1 M146V and PS1 H163Y mutations compared with controls (p < 0.01 and p < 0.05, respectively). No differences were seen between cell lines with and without the Swedish APP KM670/671NL double mutation. We suggest that various gene mutations associated with AD have different consequences for the regulation of adenylyl cyclase signal transduction in this disorder.

Original languageEnglish
Pages (from-to)2031-2035
Number of pages5
JournalNeuroReport
Volume8
Issue number8
DOIs
Publication statusPublished - 1997
Externally publishedYes

Keywords

  • Adenylyl cyclase
  • Alzheimer's disease
  • Amyloid precursor protein
  • Fibroblast
  • Presenilin
  • β- Adrenoceptor

ASJC Scopus subject areas

  • General Neuroscience

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