Jul 1, 2015

The impact of luteinizing hormone and testosterone on beta amyloid (Aβ) accumulation: Animal and human clinical studies

Hormones and Behavior
Giuseppe VerdileRalph N Martins

Abstract

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.

  • References87
  • Citations6

Mentioned in this Paper

Metabolic Process, Cellular
SHBG
Study
Familial Alzheimer Disease (FAD)
Pathogenic Aspects
Androgen Receptor
Biochemical Pathway
Testosterone Measurement
Recombinant Gonadotropin
Pathogenesis

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