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Background <p>Neuroinflammation and glial dysfunction are increasingly recognized as key contributors to Parkinson’s disease (PD) pathology. However, the relationship between circulating neurodegeneration-related biomarkers and freezing of gait (FOG), a disabling motor complication, remains unclear.</p> Results <p>This cross-sectional study included 46 PD patients (22 with FOG, 24 without) and 14 age- and sex-matched controls. Serum concentrations of neurofilament light chain (NfL), glial fibrillary acidic protein (GFAP), soluble triggering receptor expressed on myeloid cells-2 (sTREM-2), and neuregulin-1 (NRG-1) were measured via ELISA. A composite Inflammatory Load Index (ILI) was constructed from CRP, ESR, NLR, HDL, and uric acid values. Clinical severity was assessed using Unified Parkinson’s Disease Rating Scale (UPDRS), Hoehn and Yahr (HY) scale, Parkinson’s Disease Questionnaire-39 (PDQ-39), and the Freezing of Gait Questionnaire (FOG-Q) scales.Compared with controls, PD patients showed significantly elevated serum NfL and GFAP levels and reduced NRG-1 levels (all <i>p</i> &lt; 0.01). Within PD, no significant differences were observed for NfL, GFAP, or sTREM-2 between freezing and non-freezing subgroups. Interestingly, serum NRG-1 levels were higher in the FOG group (<i>p</i> = 0.031) despite comparable inflammatory indices. In adjusted models, NRG-1 showed a significant main effect for FOG status (F(1, 37) = 4.65, <i>p</i> = 0.037).</p> Conclusion <p>These findings highlight distinct peripheral biomarker signatures in PD, indicating widespread axonal and astroglial injury alongside impaired trophic signaling. The elevated NRG-1 levels in FOG may represent a phenotype-specific, compensatory neuroprotective response rather than a marker of inflammation. Future longitudinal studies integrating serum and CSF biomarkers with imaging and mechanistic analyses are warranted to validate these observations.</p>

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Peripheral neurodegenerative and neuroprotective biomarker signatures in Parkinson’s disease with and without freezing of gait

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月18日

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  • Yagmur Inalkac Gemici,
  • Melike Batum,
  • Fatih Celik,
  • Zeynep Zerrin Goz,
  • Muhammed Nurullah Yigit,
  • Cevval Ulman,
  • Hatice Maviogöu

摘要

Background

Neuroinflammation and glial dysfunction are increasingly recognized as key contributors to Parkinson’s disease (PD) pathology. However, the relationship between circulating neurodegeneration-related biomarkers and freezing of gait (FOG), a disabling motor complication, remains unclear.

Results

This cross-sectional study included 46 PD patients (22 with FOG, 24 without) and 14 age- and sex-matched controls. Serum concentrations of neurofilament light chain (NfL), glial fibrillary acidic protein (GFAP), soluble triggering receptor expressed on myeloid cells-2 (sTREM-2), and neuregulin-1 (NRG-1) were measured via ELISA. A composite Inflammatory Load Index (ILI) was constructed from CRP, ESR, NLR, HDL, and uric acid values. Clinical severity was assessed using Unified Parkinson’s Disease Rating Scale (UPDRS), Hoehn and Yahr (HY) scale, Parkinson’s Disease Questionnaire-39 (PDQ-39), and the Freezing of Gait Questionnaire (FOG-Q) scales.Compared with controls, PD patients showed significantly elevated serum NfL and GFAP levels and reduced NRG-1 levels (all p < 0.01). Within PD, no significant differences were observed for NfL, GFAP, or sTREM-2 between freezing and non-freezing subgroups. Interestingly, serum NRG-1 levels were higher in the FOG group (p = 0.031) despite comparable inflammatory indices. In adjusted models, NRG-1 showed a significant main effect for FOG status (F(1, 37) = 4.65, p = 0.037).

Conclusion

These findings highlight distinct peripheral biomarker signatures in PD, indicating widespread axonal and astroglial injury alongside impaired trophic signaling. The elevated NRG-1 levels in FOG may represent a phenotype-specific, compensatory neuroprotective response rather than a marker of inflammation. Future longitudinal studies integrating serum and CSF biomarkers with imaging and mechanistic analyses are warranted to validate these observations.