Revisiting the Effect of Leptin on Alzheimer Disease and Parkinson Disease: The Role of Insulin Sensitivity
Authors' conclusion
The study offers evidence supporting a potential protective effect of leptin in AD, but not PD, via the enhancement of insulin sensitivity. Our findings underscore the distinct roles of leptin in AD and PD.
Study context
- Population
- Genome-wide association studies summary-level data on leptin, soluble leptin receptor (sLEPR), Alzheimer disease (AD) and Parkinson disease (PD)
- Comparison
- Genetically proxied higher leptin and sLEPR levels vs AD and PD risk
- Outcome
- Causal effect of leptin and sLEPR on AD and PD (inverse variance-weighted method)
Methodological detailsgenome-wide association studies summary-level data, multivariable Mendelian randomization (MR), inverse variance-weighted method (primary analysis)
- Genome-wide association studies summary-level data
- Multivariable MR
- Inverse variance-weighted method (primary analysis)
Main finding
As reported in the abstract
Higher leptin and AD risk, OR
0.838
95% CI 0.741–0.948P = .005
Further findings
Leptin effect on AD after adjustment for insulin sensitivity index (ISI) (multivariable MR)
- Attenuated to null after ISI adjustment, OR
- 0.879 (95% CI 0.758-1.018, P = .086)
- Not attenuated after body mass index (BMI) adjustment
Reverse causation: AD and PD on leptin and sLEPR levels
- No causal impact of AD and PD on circulating leptin and sLEPR
Sensitivity analyses
- Robust associations, no obvious pleiotropy and heterogeneity
Original publication
Revisiting the Effect of Leptin on Alzheimer Disease and Parkinson Disease: The Role of Insulin Sensitivity. J Clin Endocrinol Metab. Published 5 March 2024. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →