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

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    Fulltext not available
    Authors
    Verdile, Giuseppe
    Asih, P.
    Barron, A.
    Wahjoepramono, E.
    Ittner, L.
    Martins, R.
    Date
    2015
    Type
    Journal Article
    
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    Citation
    Verdile, G. and Asih, P. and Barron, A. and Wahjoepramono, E. and Ittner, L. and Martins, R. 2015. The impact of luteinizing hormone and testosterone on beta amyloid (Aß) accumulation: Animal and human clinical studies. Hormones and Behavior.
    Source Title
    Hormones and Behavior
    DOI
    10.1016/j.yhbeh.2015.05.020
    ISSN
    0018-506X
    School
    School of Biomedical Sciences
    URI
    http://hdl.handle.net/20.500.11937/26923
    Collection
    • Curtin Research Publications
    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 (Aß) in the brain, which has a key role in the neurodegenerative cascade. Both testosterone and LH have been shown to modulate CNS Aß accumulation in animal studies, and associations with cerebral amyloid load in human studies have supported this. The underlying mechanisms by which these hormones modulate Aß accumulation and contribute to neurodegeneration are not completely understood, however they have been shown to regulate Aß 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 Aß and provide an update on therapeutic approaches targeting these hormones.

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