Defective phorbol ester-stimulated secretion of β-amyloid precursor protein from Alzheimer's disease fibroblasts

Stefania Bergamaschi, Giuliano Binetti, Stefano Govoni, William C. Wetsel, Fiorenzo Battaini, Marco Trabucchi, Angelo Bianchetti, Marco Racchi

Research output: Contribution to journalArticle

Abstract

The present study shows that cultured fbroblasts 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 EC50 twofold higher than control fibroblasts. Furthermore, we observed that such defective regulation of the amyloid precursor secretion can possibly be correlated to a specific defect in protein kinase Cα in fibroblasts from Alzheimer patients.

Original languageEnglish
Pages (from-to)1-4
Number of pages4
JournalNeuroscience Letters
Volume201
Issue number1
DOIs
Publication statusPublished - Dec 1 1995

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Keywords

  • Alzheimer's disease
  • Amyloid precursor protein
  • Human skin fibroblasts
  • Phorbol esters
  • Protein kinase C

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Bergamaschi, S., Binetti, G., Govoni, S., Wetsel, W. C., Battaini, F., Trabucchi, M., Bianchetti, A., & Racchi, M. (1995). Defective phorbol ester-stimulated secretion of β-amyloid precursor protein from Alzheimer's disease fibroblasts. Neuroscience Letters, 201(1), 1-4. https://doi.org/10.1016/0304-3940(95)12168-4