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Mendelian randomization Bayesian model averaging (MR\u2010BMA),\n                      <jats:italic>cis\u2010<\/jats:italic>\n                      multivariable Mendelian randomization (\n                      <jats:italic>cis<\/jats:italic>\n                      \u2010MVMR), and two\u2010step\n                      <jats:italic>cis\u2010<\/jats:italic>\n                      MR assessed 11 metabolic and inflammatory mediators, and tissue\u2010specific\n                      <jats:italic>cis\u2010<\/jats:italic>\n                      MVMR identified the causal tissue.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS<\/jats:title>\n                    <jats:p>\n                      <jats:italic>GLP\u20101R<\/jats:italic>\n                      expression was associated with lower AD risk and cerebrospinal fluid phosphorylated tau (p\u2010tau) levels. The\n                      <jats:italic>cis\u2010<\/jats:italic>\n                      MVMR identified systolic blood pressure as the only independent mediator, whereas\n                      <jats:italic>GLP\u20101R<\/jats:italic>\n                      retained a direct protective effect on AD. Tissue\u2010specific\n                      <jats:italic>cis\u2010<\/jats:italic>\n                      MVMR attributed the effect predominantly to cortical (posterior inclusion probability [PIP]\u00a0=\u00a00.998) rather than blood\n                      <jats:italic>GLP\u20101R<\/jats:italic>\n                      expression (PIP\u00a0=\u00a00.002).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSION<\/jats:title>\n                    <jats:p>\n                      Genetic evidence supports\n                      <jats:italic>GLP\u20101R<\/jats:italic>\n                      as a potential target in AD, with a protective effect not fully explained by peripheral metabolic improvement and possibly involving cortical neuroprotection, supporting further investigation of brain\u2010penetrant agents at preclinical or prodromal stages.\n                    <\/jats:p>\n                  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