Antigonadotropins: A Novel Strategy to Halt Alzheimers Disease Progression

Christopher   W.   Gregory; Craig   S.   Atwood; Mark   A.   Smith; Richard   L.   Bowen

doi:10.2174/138161206775474288

Abstract

A significant amount of research has been focused on the relationship between hormones and Alzheimers disease. However, the majority of this work has been on estrogen and more recently testosterone. A serendipitous patient encounter led one of us (RLB) to question whether other hormones of the hypothalamic-pituitary-gonadal axis could be playing a role in the pathogenesis of Alzheimers disease. The age-related decline in reproductive function results in a dramatic decrease in serum estrogen and testosterone concentrations and an equally dramatic compensatory increase in serum luteinizing hormone concentrations. Indeed, there is growing evidence that the gonadotropin, luteinizing hormone, which regulates serum estrogen and testosterone concentrations, could be an important causative factor in the development of Alzheimers disease. This review provides information supporting the "gonadotropin hypothesis, " puts forth a novel mechanism of how changes in serum luteinizing hormone concentrations could contribute to the pathogenesis of Alzheimers disease, and discusses potential therapeutic anti-gonadotropin compounds.

Keywords: Luteinizing hormone (LH), follicle-stimulating hormone (FSH), Alzheimer's disease, gonadotropin releasing hormone (GnRH), cell cycle, estrogen

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