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dc.contributor.authorBarron, A.
dc.contributor.authorVerdile, Giuseppe
dc.contributor.authorMartins, R.
dc.date.accessioned2017-01-30T11:14:12Z
dc.date.available2017-01-30T11:14:12Z
dc.date.created2015-09-29T01:51:53Z
dc.date.issued2006
dc.identifier.citationBarron, A. and Verdile, G. and Martins, R. 2006. The role of gonadotoprins in Alzheimer’s disease: potential neurodegenerative mechanisms. Endocrine. 29 (2): pp. 257-269.
dc.identifier.urihttp://hdl.handle.net/20.500.11937/9656
dc.identifier.doi10.1385/ENDO:29:2:257
dc.description.abstract

In addition to the classical role of gonadotropins as a modulator of sex hormone production, it is now becoming apparent that the gonadotropins may have actions within the central nervous system. Evidence is also mounting that age-related increases in levels of the gonadotropin, luteinizing hormone (LH), may exert neuro degenerative effects such as those seen in key cellular and biochemical processes that contribute to the pathogenesis of AD. These processes include the altered metabolism of key proteins in AD pathology, beta amyloid (Aß), and its parent molecule, the amyloid precursor protein (APP). Evidence in the literature suggests that gonadotropins may be involved in processes that contribute to the etiology/pathogenesis of AD such as inflammation, cholesterol homeostasis, and insulin status. Here we examine the potential mechanisms by which gonadotropins could influence neurodegenerative processes. The role of gonadotropins in the brain and potential direct neuropathological effects of elevated gonado tropin levels is an exciting new topic in neuroendocrinology that in turn will lead to the development of novel therapeutic approaches for AD.

dc.publisherHumana Press
dc.titleThe role of gonadotoprins in Alzheimer’s disease: potential neurodegenerative mechanisms
dc.typeJournal Article
dcterms.source.volume29
dcterms.source.number2
dcterms.source.startPage257
dcterms.source.endPage269
dcterms.source.issn1355-008X
dcterms.source.titleEndocrine
curtin.accessStatusFulltext not available


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