Estrogen reduces neuronal generation of Alzheimer beta-amyloid peptides. Academic Article uri icon

Overview

abstract

  • Alzheimer's disease (AD) is characterized by the accumulation of cerebral plaques composed of 40- and 42-amino acid beta-amyloid (Abeta) peptides, and autosomal dominant forms of AD appear to cause disease by promoting brain Abeta accumulation. Recent studies indicate that postmenopausal estrogen replacement therapy may prevent or delay the onset of AD. Here we present evidence that physiological levels of 17beta-estradiol reduce the generation of Abeta by neuroblastoma cells and by primary cultures of rat, mouse and human embryonic cerebrocortical neurons. These results suggest a mechanism by which estrogen replacement therapy can delay or prevent AD.

authors

  • Xu, Huaxi
  • Gouras, G K
  • Greenfield, Jeffrey P.
  • Vincent, Bruno
  • Naslund, Jan
  • Mazzarelli, Louis
  • Fried, Gabriel
  • Jovanovic, J N
  • Seeger, Mary
  • Relkin, N R
  • Liao, Fang
  • Checler, Frédéric
  • Buxbaum, J D
  • Chait, B T
  • Thinakaran, Gopal
  • Sisodia, S S
  • Wang, Rong
  • Greengard, Paul
  • Gandy, Sam

publication date

  • April 1, 1998

Research

keywords

  • Amyloid beta-Peptides
  • Amyloid beta-Protein Precursor
  • Cerebral Cortex
  • Estradiol
  • Neurons

Identity

Scopus Document Identifier

  • 0031946864

Digital Object Identifier (DOI)

  • 10.1038/nm0498-447

PubMed ID

  • 9546791

Additional Document Info

volume

  • 4

issue

  • 4