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A limitation of these studies has been a focus on non\u2010Hispanic white participants. Despite evidence that AD prevalence, progression, and biomarkers differ across ethnoracial groups, it remains unclear whether previously identified metabolic dysregulation in AD brains generalizes across populations.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS<\/jats:title>\n                    <jats:p>We analyzed metabolomics data from 547 postmortem brain tissue samples of Hispanic American, Non\u2010Hispanic African American, and White subjects, providing the largest multiethnic AD brain cohort to date. A metabolome\u2010wide association study examined how relationships between metabolite abundance and AD neuropathology varied by ethnoracial group.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS<\/jats:title>\n                    <jats:p>Forty\u2010eight metabolites exhibited significant heterogeneity with tau pathology (Braak stage), with enrichment in tricarboxylic\u2010acid\u2010cycle intermediates and sphingolipid\u2010ceramide pathway lipids, and with metabolite\u2013tau associations driven predominantly by the Hispanic American and non\u2010Hispanic White groups.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>DISCUSSION<\/jats:title>\n                    <jats:p>These findings reveal ethnoracial\u2010specific metabolic signatures of tau pathology and emphasize the need to evaluate emerging therapeutic targets across diverse groups.<\/jats:p>\n                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