Dehydroepiandrosterone (DHEA) increases production and release of Alzheimer's amyloid precursor protein

H. D. Danenberg*, R. Haring, A. Fisher, Z. Pittel, D. Gurwitz, E. Heldman

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


Dehydroepiandrosterone (DHEA), the major secretory product of the human adrenal cortex, significantly declines with advanced age. We have previously demonstrated that DHEA prevents the reduction in non-amyloidogenic APP processing, following prolonged stimulation of the muscarinic receptor, in PC12 cells that express the m1 acetylcholine-receptor. The present study examined whether this effect may be mediated via modulation of APP metabolism. It was found that DHEA treatment increases the content of membrane-associated APP holoprotein by 24%, and the accumulation of secreted APP in the medium by 63%. No increase in viable cell number nor in nonspecific protein production was observed in DHEA-treated cells. Thus, DHEA seems to increase specifically both APP synthesis and secretion. We propose that the age-associated decline in DHEA levels may be related to the pathological APP metabolism observed in Alzheimer's disease.

Original languageEnglish
Pages (from-to)1651-1657
Number of pages7
JournalLife Sciences
Issue number19
StatePublished - 4 Oct 1996


  • Alzheimer's disease
  • PC12 cells
  • amyloid precursor protein
  • dehydroepiandrosterone


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