Herpes simplex virus and Alzheimer's disease: a Mendelian randomization study
Man Ki Kwok1, Catherine Mary Schooling2
1School of Public Health, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong Special Administrative Region, China.
Neurobiology of Aging
|November 3, 2020
Summary
Herpes simplex virus (HSV) infection is not a genetically valid target for late-onset Alzheimer's disease (AD). This Mendelian randomization study found no significant genetic link between HSV and AD risk, questioning its relevance for AD interventions.
Area of Science:
- Neuroscience
- Infectious Diseases
- Genetics
- Epidemiology
Background:
- Emerging evidence suggests a potential link between herpes simplex virus (HSV) infection and Alzheimer's disease (AD) pathogenesis.
- Investigating the causal role of infections in neurodegenerative diseases is crucial for developing effective prevention and treatment strategies.
- Genetic epidemiology offers powerful tools to assess causality, distinguishing correlation from causation.
Purpose of the Study:
- To determine if herpes simplex virus (HSV) infection represents a genetically valid target for late-onset Alzheimer's disease (AD).
- To assess the potential causal relationship between genetically predicted HSV infection and cognitive function or AD risk using Mendelian randomization.
Main Methods:
- A two-sample Mendelian randomization (MR) study was conducted.
- Genome-wide association study (GWAS) data for HSV infection (n=450,581), cognitive function (n=300,486), and late-onset AD (n=455,258) were utilized.
- Strong and independent genetic variants associated with HSV infection were used as instrumental variables to predict exposure.
Main Results:
- Genetically predicted HSV infection showed no significant association with cognitive function (mean difference = 0.0004, 95% CI: -0.001 to 0.001).
- Genetically predicted HSV infection was not associated with late-onset AD risk (OR = 0.999, 95% CI: 0.998-1.001).
- Sensitivity analyses using different genetic variant selections yielded consistent results, reinforcing the primary findings.
Conclusions:
- Herpes simplex virus (HSV) infection does not appear to be a genetically valid target for intervention in late-onset Alzheimer's disease (AD).
- The findings suggest that the relevance of HSV infection to late-onset AD may need re-evaluation, particularly from a genetic causality perspective.
- Further research should explore alternative etiological factors and therapeutic targets for Alzheimer's disease.
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