ArticleJournal of Alzheimer's disease reports
Association between genetically proxied PPARG activation and early onset Alzheimer's disease: A drug target Mendelian randomization study.
Article in Journal of Alzheimer's disease reports. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Investigating the impact of aspartame on Alzheimer's disease through network toxicology and molecular docking.Frontiers in nutrition · 2025Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Early-onset Alzheimer's disease (EOAD), which has an onset before the age of 65, is overshadowed by the more prevalent late-onset Alzheimer's disease (LOAD). Nevertheless, rather than being merely a form of LOAD that occurs at a prematurely defined younger age, EOAD differs from LOAD in multiple ways. Given these disparities, understanding the potential treatment options for EOAD becomes crucial. Objective: We aim to assess anti-diabetic drugs' potential utility in treating EOAD and LOAD from a novel perspective via drug-targeted Mendelian randomization (MR) analysis. Methods: Through Summary-data-based MR (SMR) and inverse-variance-weighted MR (IVW-MR) analysis, we assessed the associations between anti-diabetic drug targets (including DPP-4 inhibitor, Thiazolidinedione, GLP1R agonist, Sulfonylureas, SLC5A2 inhibitor, and Insulin/Insulin analog) and AD outcomes (EOAD and LOAD). We utilized two types of genetic instruments to represent the exposure to anti-diabetic drugs: eQTLs of genes encoding drug target proteins and genetic variants within or near genes encoding these target proteins associated with HbA1c from genome-wide association studies. Results: SMR analysis showed that enhanced PPARG gene expression in the blood was a protective factor for EOAD (OR = 0.733, 95%CI = 0.548-0.979, Conclusions: This study suggests that Thiazolidinedione therapy could help suppress the development of EOAD, supporting further exploration of PPARG-targeted anti-diabetic drug development.
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