Androgen receptor gene and sex-specific Alzheimer's disease

Abstract Women are at a 2-fold risk of developing late-onset Alzheimer's disease (AD) (onset at 65 years of age or older) compared with men. During perimenopausal years, women undergo hormonal changes that are accompanied by metabolic, cardiovascular, and inflammatory changes. These all togethe...

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Bibliographic Details
Published in:Neurobiology of aging 2013-08, Vol.34 (8), p.2077.e19-2077.e20
Main Authors: Ferrari, Raffaele, Dawoodi, Saad, Raju, Merrill, Thumma, Avinash, Hynan, Linda S, Maasumi, Shirin Hejazi, Reisch, Joan S, O'Bryant, Sid, Jenkins, Marjorie, Barber, Robert, Momeni, Parastoo
Format: Article
Language:English
Subjects:
Age of Onset
Aged
Aged, 80 and over
Aging
Alzheimer Disease - epidemiology
Alzheimer Disease - etiology
Alzheimer Disease - genetics
Alzheimer's disease
Androgen receptor
Chromosomes, Human, X - genetics
Cohort Studies
Epigenetics
Exons - genetics
Female
Gene Silencing
Genetic Predisposition to Disease - genetics
Humans
Internal Medicine
Male
Menopause
Neurology
Perimenopause - genetics
Perimenopause - physiology
Receptors, Androgen - genetics
Risk Factors
Sex Factors
Trinucleotide Repeats - genetics
X-inactivation
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Summary:Abstract Women are at a 2-fold risk of developing late-onset Alzheimer's disease (AD) (onset at 65 years of age or older) compared with men. During perimenopausal years, women undergo hormonal changes that are accompanied by metabolic, cardiovascular, and inflammatory changes. These all together have been suggested as risk factors for late-onset AD. However, not all perimenopausal women develop AD; we hypothesize that certain genetic factors might underlie the increased susceptibility for developing AD in postmenopausal women. We investigated the Androgen Receptor gene ( AR ) in a clinical cohort of male and female AD patients and normal control subjects by sequencing all coding exons and evaluating the length and distribution of the CAG repeat in exon 1. We could not establish a correlation between the repeat length, sex, and the disease status, nor did we identify possible pathogenic variants. AR is located on the X chromosome; to assess its role in AD, X-inactivation patterns will need to be studied to directly correlate the actual expressed repeat length to a possible sex-specific phenotypic effect.
ISSN:0197-4580
1558-1497
DOI:10.1016/j.neurobiolaging.2013.02.017