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Chemical Andropause and Amyloid-β Peptide

Sam Gandy, MD, PhD; Osvaldo P. Almeida, MD, PhD, FRANZCP; Justin Fonte, MSc; David Lim, MBBS; Anna Waterrus; Nigel Spry, MBBS, FRACP; Leon Flicker, MD, PhD, FRACP; Ralph N. Martins, PhD
JAMA. 2001;285(17):2195-2196. doi:10.1001/jama.285.17.2195-a.
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To the Editor: Estrogen status appears to modify the risk of developing Alzheimer disease (AD).1 It has recently been proposed that this may be due to the effect of gonadal hormones on amyloid-β peptide (Aβ), which is the main neurotoxic component of cerebral amyloid found in AD.24 Furthermore, rising plasma Aβ levels have been found to be associated with incipient AD,5 and a genetically linked phenotype of elevated plasma Aβ levels appears to be related to the risk for late-onset AD.6 We studied the effect of gonadal hormone withdrawal in men on plasma levels of Aβ1-40.

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Figure. Plasma Concentrations of Amyloid-β Peptide (Aβ), Testosterone, and 17β-Estradiol From 6 Men With Adenocarcinoma of the Prostate
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Plasma concentrations were determined serially on samples drawn 1 week prior to initiating treatment with flutamide and leuprorelin acetate and on weeks 4, 12, and 24.



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