Scholarlink

<p>Mitochondrial dysfunction is central to Parkinson’s disease (PD), but assessing it in vivo remains challenging. Plasma L1CAM-immunocaptured putative neuron-derived exosomes (NDEs) offer minimally invasive access to brain molecular signatures. This study investigated whether mitochondrial complex (MC) proteins in NDEs are altered in PD and explored their association with clinical features. Plasma putative NDEs were isolated from 28 patients with PD and 33 normal controls (NCs) by L1CAM immunocapture. Levels of mitochondrial subunits—NDUFS3 (Complex I), UQCRC2 (Complex III), MT-CO1 (Complex IV), and ATP5F1A (Complex V)—and the antioxidant enzyme SOD1 were quantified by ELISA. Correlations with clinical severity and diagnostic performance were analyzed. Compared with NCs, PD patients exhibited significantly lower levels of NDUFS3 and UQCRC2 in NDEs (<i>p</i> &lt; 0.05, after FDR correction). NDUFS3, UQCRC2, and SOD1 showed modest inverse correlations with motor symptom severity (<i>R</i> = −0.26). The NDUFS3/UQCRC2 combination yielded an AUC of 0.763 (95% CI: 0.638–0.862) with 100% sensitivity and 51.5% specificity in this exploratory cohort, indicating limited discriminative capacity. These exploratory findings suggest that mitochondrial proteins within plasma putative NDEs may reflect neuronal mitochondrial alterations in PD. The NDUFS3/UQCRC2 combination represents a candidate signature warranting validation in larger cohorts.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Mitochondrial Proteins in Putative Neuron-Derived Plasma Exosomes Are Altered in Parkinson’s Disease: An Exploratory Study

  • 期刊论文

  • 发表日期：

    2026年1月1日

查看全文
  • Yunxia Yao,
  • Yuan Li,
  • Chunsong Zhao,
  • Qian Yu,
  • Qimeng Li,
  • Wei Mao,
  • Lifang Zhao,
  • Yanning Cai

摘要

Mitochondrial dysfunction is central to Parkinson’s disease (PD), but assessing it in vivo remains challenging. Plasma L1CAM-immunocaptured putative neuron-derived exosomes (NDEs) offer minimally invasive access to brain molecular signatures. This study investigated whether mitochondrial complex (MC) proteins in NDEs are altered in PD and explored their association with clinical features. Plasma putative NDEs were isolated from 28 patients with PD and 33 normal controls (NCs) by L1CAM immunocapture. Levels of mitochondrial subunits—NDUFS3 (Complex I), UQCRC2 (Complex III), MT-CO1 (Complex IV), and ATP5F1A (Complex V)—and the antioxidant enzyme SOD1 were quantified by ELISA. Correlations with clinical severity and diagnostic performance were analyzed. Compared with NCs, PD patients exhibited significantly lower levels of NDUFS3 and UQCRC2 in NDEs (p < 0.05, after FDR correction). NDUFS3, UQCRC2, and SOD1 showed modest inverse correlations with motor symptom severity (R = −0.26). The NDUFS3/UQCRC2 combination yielded an AUC of 0.763 (95% CI: 0.638–0.862) with 100% sensitivity and 51.5% specificity in this exploratory cohort, indicating limited discriminative capacity. These exploratory findings suggest that mitochondrial proteins within plasma putative NDEs may reflect neuronal mitochondrial alterations in PD. The NDUFS3/UQCRC2 combination represents a candidate signature warranting validation in larger cohorts.