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<p>Magnetic resonance imaging and circulating molecular testing are potential methods for diagnosing and treating Parkinson’s disease (PD). However, their relationships remain insufficiently studied. Using genome-wide association summary statistics, we found in the general population a genetic negative correlation between white matter tract mean diffusivity and PD (-0.17 &lt; Rg &lt; -0.11, <i>p</i> &lt; 0.05), and a positive correlation with intracellular volume fraction (0.12 &lt; Rg &lt; 0.2, <i>p</i> &lt; 0.05). Additionally, 1345 circulating genes causally linked with white matter tract diffusivity were enriched for muscle physiological abnormalities (padj &lt; 0.05). Notable genes, including LRRC37A4P (effect size = 15.7, <i>p</i> = 1.23E-55) and KANSL1-AS1 (effect size = -15.3, <i>p</i> = 1.13E-52), were directly associated with PD. Moreover, 23 genes were found linked with genetically correlated PD-IDP pairs (PPH4 &gt; 0.8), including SH2B1 and TRIM10. Our study bridges the gap between molecular genetics, neuroimaging, and PD pathology, and suggests novel targets for diagnosis and treatment.</p>

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Genetic analyses identify circulating genes related to brain structures associated with Parkinson’s disease

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年1月14日

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  • Zhe Han,
  • Yanping Zhu,
  • Zhenhong Xia,
  • Qing Deng,
  • Hongjie He,
  • Quanting Yin,
  • Hui Zhang,
  • Mudan Yuan,
  • Chunhua Yang,
  • Geng Tian,
  • Jia Mi,
  • Fuyi Xu

摘要

Magnetic resonance imaging and circulating molecular testing are potential methods for diagnosing and treating Parkinson’s disease (PD). However, their relationships remain insufficiently studied. Using genome-wide association summary statistics, we found in the general population a genetic negative correlation between white matter tract mean diffusivity and PD (-0.17 < Rg < -0.11, p < 0.05), and a positive correlation with intracellular volume fraction (0.12 < Rg < 0.2, p < 0.05). Additionally, 1345 circulating genes causally linked with white matter tract diffusivity were enriched for muscle physiological abnormalities (padj < 0.05). Notable genes, including LRRC37A4P (effect size = 15.7, p = 1.23E-55) and KANSL1-AS1 (effect size = -15.3, p = 1.13E-52), were directly associated with PD. Moreover, 23 genes were found linked with genetically correlated PD-IDP pairs (PPH4 > 0.8), including SH2B1 and TRIM10. Our study bridges the gap between molecular genetics, neuroimaging, and PD pathology, and suggests novel targets for diagnosis and treatment.