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- W4311665767 abstract "Metformin, a diabetes drug with anti-aging cellular responses, has complex actions that may alter dementia onset. Mixed results are emerging from prior observational studies. To address this complexity, we deploy a causal inference approach accounting for the competing risk of death in emulated clinical trials using two distinct electronic health record systems. In intention-to-treat analyses, metformin use associates with lower hazard of all-cause mortality and lower cause-specific hazard of dementia onset, after accounting for prolonged survival, relative to sulfonylureas. In parallel systems pharmacology studies, the expression of two AD-related proteins, APOE and SPP1, was suppressed by pharmacologic concentrations of metformin in differentiated human neural cells, relative to a sulfonylurea. Together, our findings suggest that metformin might reduce the risk of dementia in diabetes patients through mechanisms beyond glycemic control, and that SPP1 is a candidate biomarker for metformin's action in the brain." @default.
- W4311665767 created "2022-12-27" @default.
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- W4311665767 date "2022-12-10" @default.
- W4311665767 modified "2023-10-18" @default.
- W4311665767 title "Causal inference in medical records and complementary systems pharmacology for metformin drug repurposing towards dementia" @default.
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- W4311665767 doi "https://doi.org/10.1038/s41467-022-35157-w" @default.
- W4311665767 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36496454" @default.
- W4311665767 hasPublicationYear "2022" @default.