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 language | English |
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Pages (from-to) | 2031-2035 |
Number of pages | 5 |
Journal | NeuroReport |
Volume | 8 |
Issue number | 8 |
DOIs | |
Publication status | Published - 1997 |
Externally published | Yes |
Keywords
- Adenylyl cyclase
- Alzheimer's disease
- Amyloid precursor protein
- Aβ
- Fibroblast
- Presenilin
- β- Adrenoceptor
ASJC Scopus subject areas
- Neuroscience(all)