Book contents
- Hormones, Cognition and Dementia
- Hormones, Cognition and Dementia
- Copyright page
- Contents
- Contributors
- Preface
- Section 1 Estrogens and cognition: perspectives and opportunities in the wake of the Women's Health Initiative Memory Study
- Section 2 Varieties of estrogenic therapy
- Section 3 Potential modulators and modifiers of estrogenic effects
- Section 4 Possible genetic factors related to hormone treatment effects
- Section 5 Testosterone, estradiol and men, and sex hormone binding globulin
- Section 6 Gonadotropin effects
- Chapter 26 Involvement of gonadotropins in cognitive function: implications for Alzheimer's disease
- Chapter 27 The role of gonadotropins and testosterone in the regulation of beta-amyloid metabolism
- Chapter 28 Epilogue
- Chapter 29 Concluding remarks
- Index
- Plate Section
Chapter 26 - Involvement of gonadotropins in cognitive function: implications for Alzheimer's disease
from Section 6 - Gonadotropin effects
Published online by Cambridge University Press: 06 July 2010
- Hormones, Cognition and Dementia
- Hormones, Cognition and Dementia
- Copyright page
- Contents
- Contributors
- Preface
- Section 1 Estrogens and cognition: perspectives and opportunities in the wake of the Women's Health Initiative Memory Study
- Section 2 Varieties of estrogenic therapy
- Section 3 Potential modulators and modifiers of estrogenic effects
- Section 4 Possible genetic factors related to hormone treatment effects
- Section 5 Testosterone, estradiol and men, and sex hormone binding globulin
- Section 6 Gonadotropin effects
- Chapter 26 Involvement of gonadotropins in cognitive function: implications for Alzheimer's disease
- Chapter 27 The role of gonadotropins and testosterone in the regulation of beta-amyloid metabolism
- Chapter 28 Epilogue
- Chapter 29 Concluding remarks
- Index
- Plate Section
Summary
Casadesus and colleagues make a case that hormonal changes associated with the dysregulation of the hypothalamic-pituitary-gonadal (HPG) axis following menopause/andropause are implicated in the pathogenesis of Alzheimer's disease (AD). Experimental support for this postulate has come from studies demonstrating an increase in amyloid-β (Aβ) deposition following ovariectomy/castration. Because sex steroids and gonadotropins are both part of the HPG feedback loop, decrements in sex steroids result in a proportionate increase in gonadotropins. They provide a review of the basic science relevant to luteinizing hormone (LH) and its receptor as a background for considering LH regulation of cognitive behaviors and AD pathology. Results of their analyses suggest that marked increases in serum LH following menopause/andropause is a physiologically relevant signal that could increase Aβ secretion and deposition in the aging brain. Suppression of the age-related increase in serum gonadotropins using anti-gonadotropin agents, such as leuprolide, is proposed as a novel therapeutic strategy for AD.
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- Information
- Hormones, Cognition and DementiaState of the Art and Emergent Therapeutic Strategies, pp. 251 - 258Publisher: Cambridge University PressPrint publication year: 2009