The present study shows that cultured fibroblasts from sporadic Alzheimer's disease patients are deficient in protein kinase C-regulated secretion of amyloid precursor protein. In particular, Alzheimer fibroblasts show a reduced basal secretion and a reduced response at low concentrations of phorbol-12,13-dibutyrate, with an EC(50) twofold higher than control fibroblasts. Furthermore, we observed that such defective regulation of the amyloid precursor secretion can possibly bi: correlated to a specific defect in protein kinase C alpha in fibroblasts from Alzheimer patients.
Bergamaschi, S., Binetti, G., Govoni, S., Wetsel, W.c., Battaini, F.m., Trabucchi, M.m., et al. (1995). Defective phorbol ester-stimulated secretion of beta-amyloid precursor protein from Alzheimer's disease fibroblasts. NEUROSCIENCE LETTERS, 201(1), 1-4 [10.1016/0304-3940(95)12168-4].
Defective phorbol ester-stimulated secretion of beta-amyloid precursor protein from Alzheimer's disease fibroblasts
BATTAINI, FIORENZO MARIA;TRABUCCHI, MARCO MARIO;
1995-01-01
Abstract
The present study shows that cultured fibroblasts from sporadic Alzheimer's disease patients are deficient in protein kinase C-regulated secretion of amyloid precursor protein. In particular, Alzheimer fibroblasts show a reduced basal secretion and a reduced response at low concentrations of phorbol-12,13-dibutyrate, with an EC(50) twofold higher than control fibroblasts. Furthermore, we observed that such defective regulation of the amyloid precursor secretion can possibly bi: correlated to a specific defect in protein kinase C alpha in fibroblasts from Alzheimer patients.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.