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Chapter 17 - Apolipoprotein E, hormone therapy, and neuroprotection

from Section 4 - Possible genetic factors related to hormone treatment effects

Published online by Cambridge University Press:  06 July 2010

Eef Hogervorst
Affiliation:
Loughborough University
Victor W. Henderson
Affiliation:
Stanford University, California
Robert B. Gibbs
Affiliation:
University of Pittsburgh
Roberta Diaz Brinton
Affiliation:
University of Southern California
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Summary

Editors' introduction

Struble and McAsey propose that apolipoprotein E (APOE) is a pivotal required intermediary in the neuroprotective effects of hormone replacement therapy (HT) not only in dementia but in other chronic neurological diseases. Basic science analyses indicate that 17β-estradiol increases APOE expression, which facilitates neuronal plasticity, neural repair, and could delay progression of several types of neurodegenerative disease. The issue of the APOE4 isoform, which may be a negative regulator of HT outcomes, is considered along with therapeutic implications for either increasing or decreasing its expression. These authors propose that subsequent studies of the impact of HT or selective estrogen receptor modulators on neurological function should include APOE genotyping.

Type
Chapter
Information
Hormones, Cognition and Dementia
State of the Art and Emergent Therapeutic Strategies
, pp. 162 - 170
Publisher: Cambridge University Press
Print publication year: 2009

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