Blood proteomics of menopause map to brain aging and dementia risk

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Abstract Menopause is a hallmark process in biological aging that has been implicated in later neurodegenerative risk. We leveraged proteomics data from multiple cohorts to identify biological changes underlying menopause and its links to brain aging. In N =80 rigorously staged (STRAW+10) pre-, peri-, and postmenopausal women with serum NULISAseq proteomics, spontaneous menopause was characterized by dysregulation in inflammatory, synaptic, metabolic, and Alzheimer’s disease biologic processes, which tracked more strongly with hormones than with age. Validation analyses in age-matched pre/peri-versus postmenopausal women with plasma Olink proteomics ( N =2,814) replicated the observed proteomic shifts and revealed broader menopause-related upregulation of inflammatory and catabolic processes plus accelerated organ and cell aging, including brain aging. In four independent cohorts of older women (average age=60.7 to 72.1 years; total N =11,925), menopause-related proteomic elevations consistently associated with poorer cognitive outcomes. The molecular signatures of menopause may inform biomarkers or therapeutic targets for brain health in midlife women.

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