Mitochondrial dysfunction in a mouse model of prodromal Parkinson's disease: A metabolomic analysis

被引：2

作者：

Ikuno, Masashi ^{[1
]}

Yamakado, Hodaka ^{[1
]}

Amano, Ikuko ^{[1
]}

Hatanaka, Yusuke ^{[1
]}

Uemura, Norihito ^{[1
]}

Matsuzawa, Shu-ichi ^{[1
]}

Takahashi, Ryosuke ^{[1
]}

机构：

[1] Kyoto Univ, Dept Neurol, Grad Sch Med, Kyoto, Japan

来源：

NEUROSCIENCE LETTERS | 2021年 / 765卷

关键词：

Alpha-synuclein; Parkinson's disease; Biomarker; Prodromal Parkinson's disease; Mitochondria; Metabolome; COMPLEX-I; ALPHA-SYNUCLEIN; DNA;

D O I：

10.1016/j.neulet.2021.136267

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

For the development of disease-modifying therapies for Parkinson's disease (PD) the identification of biomarkers in the prodromal stage is urgently required. Because PD is considered a systemic disease even in the early stage, we performed a metabolomic analysis of the plasma from a mouse model of prodromal PD (p-PD). Increased levels of isobutyrylcarnitine in p-PD mice imply an abnormality in beta-oxidation in mitochondria, and increased levels of pyrimidine nucleoside can be associated with mitochondrial dysfunction. Consistent with these results, the immunoblot analysis showed a defect in mitochondrial complex I assembly in p-PD mice. These results suggest that systemic mitochondrial dysfunction may exist in p-PD mice and contribute to the pathogenesis of PD, potentially being useful as early biomarkers for PD.

引用

页数：6