Title

The Role of Gonadotropins and Testosterone in the Regulation of beta Amyloid Metabolism.

Document Type

Book Chapter

Publisher

Cambridge University Press

Faculty

Computing, Health and Science

School

Exercise, Biomedical and Health Science, Centre for Alzheimer's Disease

RAS ID

8690

Comments

This chapter was originally published as: Verdile, G. , & Martins, R. N. (2009). The role of gonadotropins and testosterone in the regulation of beta amyloid metabolism. In Hogervorst, E., Henderson, V. W., Gibbs, R. B., & Brinton, R. D. (Eds.). Hormones, Cognition and Dementia: State of the Art and Emergent Therapeutic Strategies (pp. 259-268). New York: Cambridge University Press. Original book available here

Abstract

Hormonal changes associated with ageing have been implicated in the increased risk of developing dementia and in the pathogenesis of Alzheimer’s disease (AD). Although age and the possession of the apolipoprotein 4 allele (APOE 4) are major risk factors for AD the actual trigger(s) of disease onset remain to be established. Sex hormones are considered likely candidates. Low serum levels of oestrogen in post-menopausal women and testosterone in andropausal men have been shown to be associated with AD. These hormones also play important roles in modulating beta amyloid (A) levels, the accumulation of which has a critical role in the cascade of pathogenic events that lead to neuronal degeneration in AD. It is also now becoming apparent that elevated levels of gonadotropins (particularly luteinizing hormone- LH) are also associated with increased risk of developing AD and have a role in the metabolism and accumulation of A. The complete mechanisms that underlie the effects of the sex steroids and gonadotropins on AD pathogenesis and whether one is secondary to the other or whether both have a role to play remains to be elucidated. This review focuses specifically on the sex hormone, testosterone and the gonadotropin luteinizing hormone (LH). It outlines the role of these hormones in regulating A metabolism and APP processing and discusses their potential as targets for developing effective therapeutic agents for AD.

 

Link to publisher version (DOI)

10.1017/CBO9780511635700.028