Skip to main content

Lund University Publications

LUND UNIVERSITY LIBRARIES

Estrogen reduces neuronal generation of Alzheimer β-amyloid peptides

Xu, Huaxi ; Gouras, Gunnar K. LU orcid ; Greenfield, Jeffrey P. ; Vincent, Bruno ; Naslund, Jan ; Mazzarelli, Louis ; Fried, Gabriel ; Jovanovic, Jasmina N. ; Seeger, Mary and Relkin, Norman R. , et al. (1998) In Nature Medicine 4(4). p.447-451
Abstract

Alzheimer's disease (AD) is characterized by the accumulation of cerebral plaques composed of 40- and 42-amino acid ̄-amyloid (Aβ) peptides, and autosomal dominant forms of AD appear to cause disease by promoting brain Aβ 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 17β-estradiol reduce the generation of Aβ 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.

Please use this url to cite or link to this publication:
author
; ; ; ; ; ; ; ; and , et al. (More)
; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; and (Less)
publishing date
type
Contribution to journal
publication status
published
subject
in
Nature Medicine
volume
4
issue
4
pages
447 - 451
publisher
Nature Publishing Group
external identifiers
  • pmid:9546791
  • scopus:0031946864
ISSN
1078-8956
DOI
10.1038/nm0498-447
language
English
LU publication?
no
id
1ea2a08a-e65b-4b85-bdf6-c754ddc5ff0e
date added to LUP
2020-02-20 14:29:11
date last changed
2024-04-03 03:10:34
@article{1ea2a08a-e65b-4b85-bdf6-c754ddc5ff0e,
  abstract     = {{<p>Alzheimer's disease (AD) is characterized by the accumulation of cerebral plaques composed of 40- and 42-amino acid ̄-amyloid (Aβ) peptides, and autosomal dominant forms of AD appear to cause disease by promoting brain Aβ 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 17β-estradiol reduce the generation of Aβ 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.</p>}},
  author       = {{Xu, Huaxi and Gouras, Gunnar K. and Greenfield, Jeffrey P. and Vincent, Bruno and Naslund, Jan and Mazzarelli, Louis and Fried, Gabriel and Jovanovic, Jasmina N. and Seeger, Mary and Relkin, Norman R. and Liao, Fang and Checler, Frédéric and Buxbaum, Joseph D. and Chait, Brian T. and Thinakaran, Gopal and Sisodia, Sangram S. and Wang, Rong and Greengard, Paul and Gandy, Sam}},
  issn         = {{1078-8956}},
  language     = {{eng}},
  month        = {{04}},
  number       = {{4}},
  pages        = {{447--451}},
  publisher    = {{Nature Publishing Group}},
  series       = {{Nature Medicine}},
  title        = {{Estrogen reduces neuronal generation of Alzheimer β-amyloid peptides}},
  url          = {{http://dx.doi.org/10.1038/nm0498-447}},
  doi          = {{10.1038/nm0498-447}},
  volume       = {{4}},
  year         = {{1998}},
}