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Background <p>Alzheimer’s disease (AD) and Parkinson’s disease (PD) share neuroinflammatory features, yet their common immune-related mechanisms remain unclear.</p> Methods <p>We integrated microarray datasets from AD/PD brain tissues to identify immune-related genes (IRGs). Hub genes were prioritized via protein-protein interaction (PPI) networks and validated using a Parkinson’s dementia (PDD) cohort and AD/PD mouse models. Functional enrichment, immune cell infiltration, and TF-miRNA networks were analyzed.</p> Results <p>Eleven hub IRGs (<i>CXCR4, FLT1, SLIT1/2, SEMA3G/6D</i>, etc.) were identified. <i>CXCR4</i> and <i>FLT1</i> exhibited significant upregulation in AD/PD patient brain tissues (AUC &gt; 0.7, adjusted <i>p</i>-value of &lt;0.05) and mouse model brain tissues (<i>p</i> &lt; 0.05), correlating with cytokine signaling and axon guidance pathways. <i>CXCR4</i> is uniquely associated with resting memory CD4+ T cells in both diseases, while <i>FLT1</i> showed disease-specific immune interactions. A TF-miRNA network (39 TFs, 22 miRNAs) implicated <i>CREB1</i> and <i>STAT1/3</i> as key regulators.</p> Conclusion <p><i>CXCR4</i> and <i>FLT1</i> are pivotal shared immune hubs in AD/PD, linked to T-cell dysregulation and neuroinflammation. These findings highlight potential therapeutic targets and biomarkers for neurodegenerative comorbidity.</p>

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Exploration and validation of the immune-related genes signatures and potential molecular mechanisms shared between Alzheimer’s disease (AD) and Parkinson’s disease (PD)

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年9月30日

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  • Kaige Zhou,
  • Jingxing Zhang,
  • Junhui Su,
  • Weifang Tong,
  • Ruoyu Li,
  • Xuerui Xiang,
  • Lingjing Jin,
  • Yunping Song

摘要

Background

Alzheimer’s disease (AD) and Parkinson’s disease (PD) share neuroinflammatory features, yet their common immune-related mechanisms remain unclear.

Methods

We integrated microarray datasets from AD/PD brain tissues to identify immune-related genes (IRGs). Hub genes were prioritized via protein-protein interaction (PPI) networks and validated using a Parkinson’s dementia (PDD) cohort and AD/PD mouse models. Functional enrichment, immune cell infiltration, and TF-miRNA networks were analyzed.

Results

Eleven hub IRGs (CXCR4, FLT1, SLIT1/2, SEMA3G/6D, etc.) were identified. CXCR4 and FLT1 exhibited significant upregulation in AD/PD patient brain tissues (AUC > 0.7, adjusted p-value of <0.05) and mouse model brain tissues (p < 0.05), correlating with cytokine signaling and axon guidance pathways. CXCR4 is uniquely associated with resting memory CD4+ T cells in both diseases, while FLT1 showed disease-specific immune interactions. A TF-miRNA network (39 TFs, 22 miRNAs) implicated CREB1 and STAT1/3 as key regulators.

Conclusion

CXCR4 and FLT1 are pivotal shared immune hubs in AD/PD, linked to T-cell dysregulation and neuroinflammation. These findings highlight potential therapeutic targets and biomarkers for neurodegenerative comorbidity.