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- W4311453641 abstract "Abstract Menopause has been implicated in women’s greater life-time risk for Alzheimer’s disease (AD) due to its disruptive action on multiple neurobiological mechanisms resulting in amyloid-β deposition and synaptic dysfunction.While these effects are typically attributed to declines in estradiol, mechanistic analyses implicate pituitary gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH), in AD pathology. In transgenic mouse models of AD, increasing FSH and LH accelerate amyloid-β deposition, while inhibiting these hormones prevents emergence of AD lesions and neurodegeneration. Herein, we take a translational approach to show that, among midlife women at risk for AD, FSH elevations over the menopause transition are associated with higher amyloid-β burden, and both FSH and LH increases are associated with lower gray matter volume in AD-vulnerable brain regions. Results were independent of age, hormone therapy usage, and plasma estradiol levels. These findings provide novel therapeutic targets for sex-based precision medicine strategies for AD prevention." @default.
- W4311453641 created "2022-12-26" @default.
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- W4311453641 date "2022-12-14" @default.
- W4311453641 modified "2023-10-14" @default.
- W4311453641 title "Elevated gonadotropin levels are associated with increased biomarker risk of Alzheimer’s disease in midlife women" @default.
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- W4311453641 doi "https://doi.org/10.21203/rs.3.rs-2351642/v1" @default.
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