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Generalized Anxiety Disorder (GAD) is a chronic condition characterized by excessive and uncontrollable worry that persists for at least six months, significantly interfering with daily functioning. Unlike situational anxiety, which arises in response to specific stressors, GAD often occurs without a clear cause. Individuals may experience disproportionate worry about work, health, or relationships. For instance, a person might continuously fear poor health despite normal medical evaluations or...
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Human genetics provides a profound framework for understanding the interplay between genetic predispositions and human psychology. At the heart of this discipline lies the study of how genes influence physical traits, behaviors, and susceptibility to diseases. Each person carries a unique genetic code that subtly or significantly shapes their psychological and behavioral landscape.
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Related Experiment Video

Updated: Sep 9, 2025

Social Isolation Model: A Noninvasive Rodent Model of Stress and Anxiety
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ZDHHC5 Mediates Immune Dysregulation Driving Generalized Anxiety Disorder Risk.

Fuqiang Sun1, Gengchen Lu1, Nannan Li2

  • 1College of Acupuncture and Tuina, Shandong University of Traditional Chinese Medicine, Jinan, Shandong, China.

Brain and Behavior
|September 3, 2025
PubMed
Summary
This summary is machine-generated.

This study identifies ZDHHC5 as a key gene in generalized anxiety disorder (GAD) pathogenesis. It highlights ZDHHC5

Keywords:
Mendelian randomization (MR)generalized anxiety disorder (GAD)immune cellspalmitoylation

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Area of Science:

  • Genetics
  • Immunology
  • Neuroscience

Background:

  • Generalized anxiety disorder (GAD) is a prevalent mental health condition with complex genetic underpinnings.
  • Palmitoylation, a post-translational modification, plays a role in various cellular processes, but its specific involvement in GAD remains underexplored.

Purpose of the Study:

  • To identify genes associated with palmitoylation that are implicated in GAD.
  • To investigate the mechanistic role of these genes, particularly focusing on immune cell-mediated pathways.

Main Methods:

  • Identified palmitoylation-expression quantitative trait loci (eQTL) genes by intersecting palmitoylation-related genes with genome-wide eQTL datasets.
  • Employed two-sample Mendelian randomization (MR) and summary-data-based Mendelian randomization (SMR) to establish causal relationships between eQTL genes and GAD.
  • Examined underlying mechanisms through immune cell-mediated processes.

Main Results:

  • Identified 22 palmitoylation-eQTL gene loci, with five significantly linked to GAD: PPT2, ZDHHC5, ZDHHC13, ZDHHC20, and ZDHHC24.
  • ZDHHC5 and ZDHHC13 were validated as target genes via SMR analysis.
  • Mediation MR analysis revealed that SSC-A on CD4+ T cells mediated the effect of ZDHHC5 (36.4% mediation).

Conclusions:

  • ZDHHC5 is implicated in GAD pathogenesis.
  • ZDHHC5 modulates SSC-A on CD4+ T cells, suggesting a novel immune cell-mediated mechanism in GAD.
  • These findings offer new targets for GAD pathophysiology research.