The impact of luteinizing hormone and testosterone on beta amyloid (Aβ) accumulation

animal and human clinical studies

Giuseppe Verdile*, Prita R. Asih, Anna M. Barron, Eka J. Wahjoepramono, Lars M. Ittner, Ralph N. Martins

*Corresponding author for this work

Research output: Contribution to journalArticle

17 Citations (Scopus)


This article is part of a Special Issue "SBN 2014".Hormonal changes associated with ageing have been implicated in the pathogenesis of Alzheimer's disease (AD), the most common form of dementia. Reductions in serum testosterone and increases in luteinizing hormone (LH) are established AD risk factors for dementia in men and have important roles in modulating AD pathogenesis. One of the defining features of AD is the accumulation of amyloid-beta (Aβ) in the brain, which has a key role in the neurodegenerative cascade. Both testosterone and LH have been shown to modulate CNS Aβ accumulation in animal studies, and associations with cerebral amyloid load in human studies have supported this. The underlying mechanisms by which these hormones modulate Aβ accumulation and contribute to neurodegeneration are not completely understood, however they have been shown to regulate Aβ metabolism, enhance its clearance and alter the processing of its parent molecule, the amyloid precursor protein. This review will discuss underlying mechanisms by which testosterone and LH modulate Aβ and provide an update on therapeutic approaches targeting these hormones.

Original languageEnglish
Pages (from-to)81-90
Number of pages10
JournalHormones and Behavior
Publication statusPublished - 1 Nov 2015
Externally publishedYes


  • Alzheimer's disease
  • Amyloid precursor protein beta amyloid
  • Luteinizing hormone
  • Testosterone

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