Type 2 diabetes, glycaemic traits, structural brain capacity and cognitive function: A Mendelian randomization
Manjun Luo1, Mengting Sun1, Tingting Wang1
1Department of Epidemiology and Health Statistics, Xiangya School of Public Health, Central South University, Changsha, China.
Diabetes, Obesity & Metabolism
|June 26, 2024
Summary
Genetically predicted fasting proinsulin causally impacts cognitive function, but type 2 diabetes does not. Brain imaging traits did not mediate this association, suggesting other mechanisms are involved in cognitive impairment.
Area of Science:
- Neuroscience
- Metabolic Disorders
- Genetics
Background:
- Type 2 diabetes and glycaemic traits are linked to cognitive decline.
- Understanding the causal pathways is crucial for developing interventions.
Purpose of the Study:
- To investigate causal links between type 2 diabetes, glycaemic traits, and cognitive function.
- To explore the mediating role of brain imaging-derived phenotypes (IDPs) using Mendelian randomization (MR).
Main Methods:
- Utilized publicly available summary data for univariable and multivariable MR analyses.
- Performed two-step MR analysis to assess mediation by brain IDPs.
Main Results:
- No causal association was found between type 2 diabetes and cognitive function.
- Higher genetically predicted fasting proinsulin was associated with worse cognitive performance (beta: -0.027, 95% CI -0.048, -0.005).
- Brain IDPs did not mediate the relationship between fasting proinsulin and cognitive function.
Conclusions:
- Genetically predicted fasting proinsulin has a causal effect on cognitive function.
- No investigated brain IDP acts as a mediator in this pathway.
- Further research is needed to elucidate the biological mechanisms linking fasting proinsulin to cognitive performance.
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