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<p>Schizophrenia is associated with structural and functional changes in the central nervous system, including the most distal part of it, the retina. However, the question of whether retinal atrophy is present before individuals develop schizophrenia or is a secondary consequence of the disorder remains unanswered. Here we address this question by examining the association between polygenic risk scores for schizophrenia and retinal morphologies in individuals without a schizophrenia diagnosis. We used population data for 34,939 white British and Irish individuals from the UK Biobank. Our robust regression results show that higher polygenic risk scores for schizophrenia were associated with thinner overall maculae, while controlling for confounding factors (<i>b</i> = −0.17, <i>P</i> = 0.018). Similarly, we found that greater polygenic risk scores for schizophrenia specific to neuroinflammation gene sets were associated with thinner ganglion cell inner plexiform layers (<i>b</i> = −0.10, self-contained <i>P</i> = 0.014, competitive <i>P</i> = 0.02). These results provide new evidence for genetic factors that could predispose individuals to heightened neuroinflammatory responses. Over time, these responses could contribute to neurodegenerative processes such as retinal thinning.</p>

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Genetic susceptibility to schizophrenia through neuroinflammatory pathways associated with retinal thinness

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月21日

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  • Finn Rabe,
  • Lukasz Smigielski,
  • Foivos Georgiadis,
  • Nils Kallen,
  • Wolfgang Omlor,
  • Victoria Edkins,
  • Matthias Kirschner,
  • Flurin Cathomas,
  • Edna Grünblatt,
  • Steven Silverstein,
  • Brittany Blose,
  • Daniel Barthelmes,
  • Karen Schaal,
  • Jose Rubio,
  • Todd Lencz,
  • Philipp Homan

摘要

Schizophrenia is associated with structural and functional changes in the central nervous system, including the most distal part of it, the retina. However, the question of whether retinal atrophy is present before individuals develop schizophrenia or is a secondary consequence of the disorder remains unanswered. Here we address this question by examining the association between polygenic risk scores for schizophrenia and retinal morphologies in individuals without a schizophrenia diagnosis. We used population data for 34,939 white British and Irish individuals from the UK Biobank. Our robust regression results show that higher polygenic risk scores for schizophrenia were associated with thinner overall maculae, while controlling for confounding factors (b = −0.17, P = 0.018). Similarly, we found that greater polygenic risk scores for schizophrenia specific to neuroinflammation gene sets were associated with thinner ganglion cell inner plexiform layers (b = −0.10, self-contained P = 0.014, competitive P = 0.02). These results provide new evidence for genetic factors that could predispose individuals to heightened neuroinflammatory responses. Over time, these responses could contribute to neurodegenerative processes such as retinal thinning.