Alterations in neural structure, reflected as gray matter loss, changes in metabolite levels, and alterations in water diffusion, appear in OSA. We created a linear model with sex and OSA terms and an interaction variable. Importantly, additional evidence suggests that hormone depletion occurs prior to the onset of AD and thus likely contributes to rather than results from the disease process. Also, estrogens and androgens are potent regulators of neuron viability, protecting neurons against a range of toxic insults including those implicated in AD — We created a mask for the statistical analysis to include all regions with large axonal groups including white matter, and to exclude non-brain regions and areas with very low FA, which could have high variability. The inclusion of some ventricular and purely gray matter regions likely reflects variations in spatial normalization, but the consequence of these additional regions would be only a very modest reduction in sensitivity resulting from a more stringent multiple comparisons threshold due to the slight increase in number of voxels in the search area. Sleep quality, daytime sleepiness, depression, and anxiety were assessed with questionnaires. Preprocessing The 3 later DTI series were realigned to the first series using the non-diffusion weighted b0 images; the diffusion gradient direction vectors of the images were rotated accordingly. Male and female OSA groups were matched for severity, and all 4 groups control male and female, OSA male and female were age-matched.
Corrections for eddy-current related distortions were performed using an affine coregistration. Age-related declines in brain testosterone levels in men have been described, with brain testosterone levels depleted to very low levels by 80 years of age 27 , Conversely, female 3xTgAD mice defeminized by transient neonatal testosterone treatment showed regional reductions of Abeta accumulation Areas of sex-specific, OSA-related FA reductions appeared in females relative to males, including in the bilateral cingulum bundle adjacent to the mid hippocampus, right stria terminalis near the amygdala, prefrontal and posterior-parietal white matter, corpus callosum, and left superior cerebellar peduncle. Control subjects who reported such symptoms were scheduled for a full sleep study to verify their status. Men also experience a significant age-related decrease in circulating testosterone levels, known as androgen deficiency in aging males ADAM 4. The inclusion of some ventricular and purely gray matter regions likely reflects variations in spatial normalization, but the consequence of these additional regions would be only a very modest reduction in sensitivity resulting from a more stringent multiple comparisons threshold due to the slight increase in number of voxels in the search area. We created a linear model with sex and OSA terms and an interaction variable. For example, lower plasma 17beta-estradiol E2 levels have been observed in women with AD compared to age-matched controls The b0 images were spatially normalized to the Montreal Neurological Institute MNI template, and the FA maps had the same transformation applied see Appendix A in supplemental material for details. Meanwhile, levels of both total 65 , 72 and free plasma testosterone have been observed in men with AD compared to both vascular dementia sufferers 68 and age-matched controls 64 , 67 , 73 , Further, in comparison to neuropathologically normal men, brain levels of testosterone are significantly lower not only in men with advanced AD but also in men exhibiting mild, AD-related neuropathological changes As reviewed elsewhere, estrogens and androgens increase spine density and facilitate synaptic plasticity 95 — 99 and improve select aspects of cognition 45 , — In AD, not only are brain levels of the sex hormones altered, but brain responsiveness may also be impaired as a result of altered sex hormone receptor levels and distribution. These female-specific structural changes may contribute to or derive from neuropsychological and physiological symptom differences between sexes. We review a broad literature that indicates age-related losses of estrogens in women and testosterone in men are risk factors for AD. Aging and loss of sex hormones Depletion of sex steroid hormones is an important consequence of normal aging that is associated with vulnerability to disease in hormone-responsive tissues, including the brain 4 — After verification of inclusion and exclusion criteria, the control subjects were interviewed for the presence of symptoms of OSA e. We identified regions of differing injury in male versus female OSA patients by assessing brain regions with significant interaction effects of OSA and sex on FA. Although alternations in expression and distribution of AR in AD are comparatively unexplored, a polymorphism of the androgen receptor has also been associated with AD in men Lower FA values reflect lower impedance in the plane perpendicular to the axial direction, which can result from less axonal white matter myelin, thus reflecting reduced axonal integrity. While age related decline in circulating levels of gonadally produced sex steroid hormones has been well characterized, brain levels of hormones can significantly differ from circulating levels due to sequestration by sex hormone binding globulin, the presence of brain steroid converting enzymes, and neurosteroidogenesis 24 — Interestingly, an emerging literature suggests the possibility that AD pathology may negatively feedback on steroid levels by inhibiting neurosteroidogenesis. Further, more severe cognitive deficits and beta-amyloid Abeta neuropathology have been reported in women in comparison to men 51 — 54 , although some studies have reported increased tau pathology in men 55 , Scanner limitations precluded patients with metallic implants or weight over kg.
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