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Using the Activity-based Anorexia Rodent Model to Study the Neurobiological Basis of Anorexia Nervosa
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Polygenicity at the pathway level for anorexia nervosa.

Jiayi Xu1, Jessica S Johnson2, Chaoyu Liu1,3

  • 1Department of Psychiatry, Yale School of Medicine, New Haven, CT, USA.

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Polygenic risk scores at the pathway level reveal anorexia nervosa (AN) genetic architecture. Pathway aggregation, particularly in brain and metabolism, significantly increases AN risk, improving disease prediction.

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Area of Science:

  • Genetics
  • Psychiatry
  • Computational Biology

Background:

  • Genome-wide association studies (GWAS) reveal polygenic architectures for common disorders.
  • The aggregation of genetic risk across biological pathways in complex diseases like anorexia nervosa (AN) remains poorly understood.

Purpose of the Study:

  • To investigate polygenicity at the pathway level in anorexia nervosa (AN).
  • To develop pathway-based polygenic risk scores (pathway PRS) for modeling genetic risk in AN.
  • To explore how pathway aggregation influences AN risk and prediction.

Main Methods:

  • Constructed pathway-based polygenic risk scores (pathway PRS) for 3,687 AN cases and 11,257 controls.
  • Identified AN-associated pathways using Bonferroni correction.
  • Analyzed correlations between pathway PRS, AN case proportion, and overall genetic risk.

Main Results:

  • Identified 497 AN-associated pathways across brain, metabolism, immunity, and development.
  • Observed a strong positive correlation between the number of top-ranked pathways and AN risk (r=0.74).
  • Pathway aggregation within and across functions (e.g., brain-brain, brain-metabolism) significantly increased AN risk.
  • Pathway PRS demonstrated higher AN prediction power than genome-wide PRS.

Conclusions:

  • Polygenicity operates at the pathway level, contributing to AN's complex genetic liability.
  • Pathway-level analysis offers novel insights into disease mechanisms and prediction for AN.
  • Identified specific pathway combinations associated with heightened AN risk, suggesting potential therapeutic targets.