IMR Press / FBL / Volume 13 / Issue 14 / DOI: 10.2741/3088

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Apolipoprotein E may be a critical factor in hormone therapy neuroprotection
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1 Center for Alzheimer’s Disease and Related Disorders, Department of Neurology, Southern Illinois University School of Medicine, P.O. Box 19643, Springfield, IL 62794-9643, USA
2 Biology Department, Bradley University, 1501 W. Bradley Ave., Peoria, IL 61625, USA
3 Department of Biological Sciences, Eastern Illinois University, 600 Lincoln Avenue, Charleston IL 61920, USA
4 Department of Obstetrics and Gynecology, Southern Illinois University School of Medicine, P.O. Box 19672, Springfield, IL 62794-9672, USA
Academic Editor:Kenichi Yoshida
Front. Biosci. (Landmark Ed) 2008, 13(14), 5387–5405; https://doi.org/10.2741/3088
Published: 1 May 2008
(This article belongs to the Special Issue Cell division cycle-associated genes in a chromatin context)
Abstract

In this review we examine the evidence for ovarian hormone neuroprotection in chronic neurological diseases, including stroke. We propose that neuroprotection may involve the ability of estrogens to modulate apolipoprotein E (apoE) and its receptor, the low density lipoprotein receptor related protein (LRP). Results from numerous studies have demonstrated that (1) nerve regeneration is severely delayed in apoE-gene knockout (KO) mice as compared to wild-type (WT) littermates; (2) 17beta estradiol replacement in ovariectomized mice resulted in a significant increase in levels of apoE and LRP, in the olfactory bulb (OB) and other brain areas; (3) estradiol treatment increased both apoE and neurite outgrowth in cortical and olfactory neuronal cultures; and (4) estradiol treatment had no effect on neurite outgrowth in cultures deprived of apoE or in the presence of apoE4. In essence these studies suggest that apoE is a critical intermediary for the beneficial effects of 17beta estradiol on nerve repair, which can lead to functional reorganization (plasticity). Future studies of HT should evaluate the effects of apoE genotype and production estradiol on neuroprotection.

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