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Dissecting the shared genetic architecture between anxiety and cognitive function.

Ming Yang1, Zhini Yu1, Zhengqi Wei1

  • 1Guangxi Key Laboratory of Environmental Exposomics and Entire Lifecycle Health, Guangxi Key Laboratory of Diabetic Systems Medicine, School of Public Health, Guilin Medical University, Guilin, Guangxi, 541199, China.

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Summary

This study reveals a shared genetic basis between anxiety and cognitive decline, indicating anxiety negatively impacts cognitive function through common genetic factors. Further research into these genetic links can inform future comorbidity studies.

Keywords:
AnxietyBi-directional Mendelian randomizationCognitive functionGenome-wide cross-trait analysisSummary-data-based Mendelian randomization

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Area of Science:

  • Neurogenetics
  • Psychiatric Genetics
  • Cognitive Neuroscience

Background:

  • Growing evidence links anxiety to increased cognitive decline risk.
  • The underlying genetic mechanisms of this association remain largely unknown.
  • This study investigates the shared genetic architecture and causal links between anxiety and cognitive function.

Purpose of the Study:

  • To explore the genetic correlation between anxiety and cognitive function.
  • To investigate the causal relationship between anxiety and cognitive function using bi-directional Mendelian randomization.
  • To identify shared genetic loci and functional genes implicated in both anxiety and cognitive function.

Main Methods:

  • Genome-wide association studies (GWAS) data were analyzed using linkage disequilibrium score regression (LDSC) and High-Definition Likelihood (HDL) for genetic correlation.
  • Bi-directional Mendelian randomization (MR) was employed to assess causal associations.
  • Cross-trait meta-analyses, stratified LDSC, and Summary-based MR (SMR) were used to identify shared loci and functional genes.

Main Results:

  • A significant negative genetic correlation was found between anxiety and cognitive function.
  • MR analysis supported a detrimental effect of anxiety on cognitive function (β = -0.121, P = 7.59 × 10-3).
  • Four novel shared single nucleotide polymorphisms (SNPs) were identified, with the ITIH4 gene consistently implicated. Enrichment analyses highlighted brain regions (e.g., frontal cortex) and cell types (e.g., GABAergic neurons, astrocytes).

Conclusions:

  • A common genetic foundation underlies anxiety and cognitive function, evidenced by genetic correlations and shared genes.
  • These findings offer novel insights into the comorbidity of anxiety and cognitive decline.
  • The identified genetic factors and biological pathways provide avenues for future research into their interconnectedness.