![]() The implications of this observation are that a relatively more masculine in utero development confers protection against AD for women and, relatedly, a more feminine in utero prenatal environment may predispose women to AD. This study provides the novel finding that right hand 2D:4D, a marker of prenatal androgen levels, is significantly higher in women with dementia relative to women without dementia. Largely unstudied is whether well-established differences between male and female fetuses in exposure to sex hormones impacts late life development and or manifestation of AD. There is also evidence that gender differences, including access to education, may impact sex differences in dementia risk. There is strong evidence that sex-specific patterns in the age-related depletion of estrogens and testosterone differentially contribute to increased vulnerabilities of female and male brains, respectively, to AD pathogenesis. The study was conducted under a protocol (USC UPIRB # UP-13–00035) approved by an institutional review board.Īlthough AD is characterized by numerous sex differences, the source(s) of these differences is not clearly known. The final subject pool for 2D:4D analysis consisted of 73 women (39 non-demented 34 demented) and 66 men (31 non-demented 35 demented). Further, subjects for which adequately focused hand images could not be attained were also excluded (13 excluded). Exclusion criteria were age <65 years (11 excluded) or diagnosis of non-ADRD dementia (4 excluded). A total of 167 subjects – 81 men and 86 women – participated in the study. For some persons, requested information was provided by caregivers. In subjects with a positive diagnosis of dementia, there was an additional query about the type of dementia, if known. Those with a positive history of dementia or significant memory impairment comprised the ‘demented’ group all other subjects were classified as ‘non-demented’. Participants were asked to identify their gender, provide their age, and answer whether they had been diagnosed with significant memory impairment or dementia. Under the approval and supervision of center personnel, all residents were informed of the study and welcomed to volunteer for a hand scan. Subjects were recruited from community adult care centers and assisted living facilities. This finding provides novel evidence that women with a relatively more feminine sexual differentiation may be at inherently greater risk for ADRDs. The data show that dementia in women, but not in men, is associated with significantly higher 2D:4D. To investigate the possible contribution of organizational effects of sex steroid hormones to dementia risk, we assessed right hand 2D:4D in a community sample of elderly men and women with and without dementia. Prenatal androgens induce modest but significant changes in digit length resulting in 2D:4D that, on average, are higher in women than in men. One of only a few approaches to assess differences in the in utero sex hormone milieu that drives sexual differentiation is the ratio of the lengths of the second (digit 2) and fourth (digit 4) fingers (2D:4D). Unknown is whether sex differences in ADRDs may involve organizational sex hormone actions during early sexual differentiation. Consistent with this possibility, several neurological disorders exhibit significant sex differences in prevalence and/or presentation, including autism, schizophrenia, attention deficit disorders, and yet their onsets typically occur decades prior to age-related declines in sex steroid hormones. Organizational effects of sex steroid hormones yield neural variations along a spectrum of relatively more masculine versus feminine brains that may differ in their inherent vulnerability to neural disease or its expression. In particular, increased levels of testosterone and estradiol during specific developmental periods are closely linked with sexual differentiation of the brain. In addition to their activational effects in adulthood, sex hormones also exert profound organizational effects during development. Indeed, the loss of neuroprotective effects by sex hormones is strongly linked with the regulation of multiple components of AD pathogenesis as well as increased AD risk. The most widely supported concept is that sex differences in ADRDs reflect sex-specific patterns in the age-related declines of primary sex steroid hormones, estrogens in women and androgens in men. The underlying causes of sex differences in AD and AD-related dementias (ADRDs) are uncertain. In particular, women show higher prevalence of AD than men, which may reflect in part a female bias in age-specific risks to the disease. Alzheimer’s disease (AD), the most common form of dementia, is characterized by numerous sex differences.
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