Women are at a twofold risk of developing late onset Alzheimer’s disease (LOAD) (onset ≥65 years of age) compared to 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 LOAD. 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 (AR) gene in a clinical cohort of male and female AD patients and normal controls 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, gender and the disease status, nor did we identify possible pathogenic variants. AR is located on the X chromosome; in order 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.