ArticleJournal of translational medicine2025
Chronic sleep deprivation induces plasma exosome-derived miR-150-5p downregulation as a novel mechanism involved in Parkinson's disease progression by targeting DCLK1.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Lipid Metabolism Reprogramming in the Aging Brain: Glial-Mediated Pathogenic Mechanisms and Translational Strategies in Neurodegeneration.International journal of molecular sciences · 2026Review
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10 authors.
Funding
Abstract
backgroundResearches have suggested that chronic sleep deprivation (SD) can lead to neurological dysfunction and facilitate the onset and progression of Parkinson's disease (PD). However, the association between SD and PD remains unclear. Exosome (exo) cargo comprises microRNAs (miRNAs), which are potential regulators of PD. This study focused on assessing the role and related mechanisms of SD on PD.
methodsSD plus 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mice were used to investigate effects of SD on PD. Exos were extracted from plasma by polymer precipitation method. Impacts of exos on PD were validated through intervention in 1-methyl-4-phenylpyridinium (MPP
resultsWe found that SD and SD-derived exos aggravated PD-related damage. SD-derived exos were identified as potent inducers of PD. MiR-150-5p was recognized as a key element in SD-derived exos, and doublecortin-like kinase 1 (DCLK1) was confirmed as its target gene. Supplementing miR-150-5p alleviated PD damage by inhibiting DCLK1 and abnormal α-synuclein (α-syn) expression, decreasing reactive oxygen species (ROS), p62, cleaved-caspase-3 and cleaved-caspase-9 levels, and increasing Parkin and PINK1 levels and the LC3II/I ratio.
conclusionThese findings suggested that miR-150-5p-dependent downregulation in SD-derived exos could aggravate the progression of PD via the DCLK1/α-syn pathway. MiR-150-5p decreased ROS levels, promoted mitophagy, and inhibited apoptosis, thus mitigating PD-related damage. These findings indicated that plasma-derived exos and their miRNA cargo might serve as therapeutic targets for PD, providing insights into a mechanism that links SD-related deterioration to the progression of PD.
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