The Causal Relationship between Genetically Predicted Biological Aging, Alzheimer's Disease and Cognitive Function: A
1Yu Yang, Department of Neurology and Neuroscience Center, The First Hospital of Jilin University, Jilin 130021, China. yang_yu@jlu.edu.cn.
The Journal of Prevention of Alzheimer'S Disease
|November 19, 2024
Summary
Biological aging markers like telomere length and epigenetic clocks are linked to Alzheimer's disease risk. Specific aging accelerations increase late-onset AD risk, while cognitive functions may offer protection.
Area of Science:
- Gerontology
- Neuroscience
- Genetics
Background:
- Aging is a primary risk factor for Alzheimer's disease (AD).
- Biological aging, assessed by leukocyte telomere length (LTL) and epigenetic clocks, is a key indicator of functional decline.
- The causal relationship between biological aging markers and AD risk requires further investigation.
Purpose of the Study:
- To investigate the causal links between biological aging markers and Alzheimer's disease (AD) risk.
- To explore the influence of different biological aging markers on AD subtypes (early-onset AD and late-onset AD).
- To examine the protective effects of cognitive functions against biological aging acceleration.
Main Methods:
- Mendelian randomization (MR) study design.
- Utilized the inverse-variance weighted (IVW) method for causal inference.
- Analyzed associations between biological aging markers (HannumAge, GrimAge, HorvathAge, LTL) and AD risk, considering cognitive functions (prospective memory, fluid intelligence).
Main Results:
- HannumAge acceleration and LTL shortening were associated with increased risk of late-onset AD (LOAD), but not early-onset AD (EOAD).
- Enhanced prospective memory and fluid intelligence showed potential protective effects against GrimAge acceleration.
- GrimAge and HorvathAge accelerations were found to increase LOAD risk via their effects on LTL.
Conclusions:
- Biological aging plays a significant role in AD pathogenesis.
- Specific biological aging markers differentially impact AD risk across subtypes.
- Interactions between aging markers and cognitive functions are complex and warrant further study in AD.
Keywords:
cognitive functionAlzheimer’s diseaseEpigenetic age accelerationleukocyte telomere lengthmendelian randomizationMore Related Videos
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