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<p>The gut-brain axis (GBA) plays a critical role in the pathogenesis of type 2 diabetes (T2DM) and Parkinson's disease (PD), with bidirectional communication mediated by the enteric nervous system. T2DM involves GBA dysregulation linked to insulin resistance and sustained hyperglycemia. Emerging evidence suggests a strong association between T2DM and an increased risk of PD, though the precise mechanisms remain under investigation. Proposed mechanisms include T2DM-associated gut microbiota dysbiosis, facilitated by chronic inflammation, hyperglycemia, and gut barrier dysfunction, which promotes harmful bacterial overgrowth. Epidemiological and preclinical studies suggest that this dysbiosis may contribute to PD pathogenesis via insulin resistance, impaired glucagon-like peptide 1 (GLP-1) function, and neuroinflammation. Although dietary interventions offer promising risk-reduction strategies, the core mechanisms are not fully understood. Therefore, this review aims to explore the GBA as a critical integrative pathway mediating the increased risk of PD in T2DM patients.</p>

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The Gut-Brain Axis: A Critical Link between Type 2 Diabetes and Parkinson’s disease

  • 期刊论文

  • 发表日期：

    2026年4月15日

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  • Najlaa Hamed Almohmadi,
  • Hayder M. Al-kuraishy,
  • Khulood S. Hussein,
  • Arwa M. Turkistani,
  • Fatimah M. Yousef,
  • Ali I. Al-Gareeb,
  • Ahmed M. Abdelaziz,
  • Yaser Hosny Ali Elewa,
  • Gaber El-Saber Batiha

摘要

The gut-brain axis (GBA) plays a critical role in the pathogenesis of type 2 diabetes (T2DM) and Parkinson's disease (PD), with bidirectional communication mediated by the enteric nervous system. T2DM involves GBA dysregulation linked to insulin resistance and sustained hyperglycemia. Emerging evidence suggests a strong association between T2DM and an increased risk of PD, though the precise mechanisms remain under investigation. Proposed mechanisms include T2DM-associated gut microbiota dysbiosis, facilitated by chronic inflammation, hyperglycemia, and gut barrier dysfunction, which promotes harmful bacterial overgrowth. Epidemiological and preclinical studies suggest that this dysbiosis may contribute to PD pathogenesis via insulin resistance, impaired glucagon-like peptide 1 (GLP-1) function, and neuroinflammation. Although dietary interventions offer promising risk-reduction strategies, the core mechanisms are not fully understood. Therefore, this review aims to explore the GBA as a critical integrative pathway mediating the increased risk of PD in T2DM patients.