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<p>Schizophrenia (SCZ) is a severe and chronic neuropsychiatric disorder associated with substantially shortened life expectancy and early onset of age-related comorbidities. Mounting evidence from physical health, brain structure, and cognitive function suggests that SCZ may involve accelerated biological aging. This review focuses on three core aging-related biomarkers, namely, epigenetic clocks, telomere dynamics, and the senescence-associated secretory phenotype (SASP), with the aim of systematically characterizing biological aging features in SCZ. Collectively, available studies point to altered epigenetic aging, telomere attrition, and enhanced pro-inflammatory profiles in SCZ, although findings remain inconsistent because of methodological heterogeneity, tissue specificity, and predominantly cross-sectional study designs. Oxidative stress and chronic low-grade inflammation are proposed to serve as a central hub that links these aging-related processes and may contribute to a self-sustaining pathological loop that accelerates systemic aging. Future longitudinal multi-omics studies and tissue-specific analyses are warranted to clarify causal relationships, identify dynamic aging trajectories, and explore modifiable intervention targets. Understanding the mechanistic links between SCZ and accelerated aging may provide novel insights into disease pathophysiology and facilitate the development of innovative strategies to mitigate age-related comorbidities and improve long-term health outcomes in this vulnerable population.</p>

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Accelerated aging in schizophrenia: integrating epigenetic clocks, telomere dynamics, senescence-associated secretory phenotype, and oxidative stress

  • 期刊论文

  • 发表日期：

    2026年7月11日

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  • Xuan Ge,
  • Chenying Jiang,
  • Chaoran Wu,
  • Xinyu Fang,
  • Xiangrong Zhang

摘要

Schizophrenia (SCZ) is a severe and chronic neuropsychiatric disorder associated with substantially shortened life expectancy and early onset of age-related comorbidities. Mounting evidence from physical health, brain structure, and cognitive function suggests that SCZ may involve accelerated biological aging. This review focuses on three core aging-related biomarkers, namely, epigenetic clocks, telomere dynamics, and the senescence-associated secretory phenotype (SASP), with the aim of systematically characterizing biological aging features in SCZ. Collectively, available studies point to altered epigenetic aging, telomere attrition, and enhanced pro-inflammatory profiles in SCZ, although findings remain inconsistent because of methodological heterogeneity, tissue specificity, and predominantly cross-sectional study designs. Oxidative stress and chronic low-grade inflammation are proposed to serve as a central hub that links these aging-related processes and may contribute to a self-sustaining pathological loop that accelerates systemic aging. Future longitudinal multi-omics studies and tissue-specific analyses are warranted to clarify causal relationships, identify dynamic aging trajectories, and explore modifiable intervention targets. Understanding the mechanistic links between SCZ and accelerated aging may provide novel insights into disease pathophysiology and facilitate the development of innovative strategies to mitigate age-related comorbidities and improve long-term health outcomes in this vulnerable population.