<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ye J</submitter><funding>the Open Fund Hubei Provincial Clinical Research Center for Umbilical Cord Blood Hematopoietic Stem Cells, Taihe Hospital</funding><funding>The Foundation of Health Commission of Hubei Province</funding><funding>This work was supported by the Experimental Animal Resources Development and Utilization Project of Hubei Province of China</funding><funding>Innovative research program for graduates of Hubei University of Medicine</funding><funding>Innovative Research Program of Xiangyang No.1 People&amp;apos;s Hospital</funding><funding>Innovative Research Program of Xiangyang No.1 People's Hospital</funding><pagination>567</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11401276</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>22(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Umbilical cord blood (UCB) is a rich source of multifunctional stem cells characterized by low immunogenicity. Recent research in the fields of aging and regenerative medicine has revealed the potential of human umbilical cord blood-derived exosomes (UCB-Exos) in promoting wound healing, anti-aging, and regeneration. However, their role in neurodegenerative diseases, specifically Parkinson's disease (PD), remains unexplored. This study investigates the potential therapeutic effects and underlying mechanisms of UCB-Exos on PD.&lt;h4>Methods&lt;/h4>Large extracellular vesicles (LEv), Exos, and soluble fractions (SF) of human UCB plasma were extracted to investigate their effects on motor dysfunction of the MPTP-induced PD mouse model and identify the key components that improve </pubmed_abstract><journal>Journal of nanobiotechnology</journal><pubmed_title>Umbilical cord blood-derived exosomes attenuate dopaminergic neuron damage of Parkinson's disease mouse model.</pubmed_title><pmcid>PMC11401276</pmcid><funding_grant_id>YC2024030</funding_grant_id><funding_grant_id>YC2022008</funding_grant_id><funding_grant_id>2024SCOF004</funding_grant_id><funding_grant_id>WJ2023M161</funding_grant_id><funding_grant_id>2020DFE025</funding_grant_id><funding_grant_id>YC2022003</funding_grant_id><funding_grant_id>XYY2023ZY04</funding_grant_id><funding_grant_id>YC2024017</funding_grant_id><funding_grant_id>YC2023006</funding_grant_id><pubmed_authors>Dong J</pubmed_authors><pubmed_authors>Jiang Q</pubmed_authors><pubmed_authors>Sang M</pubmed_authors><pubmed_authors>Xie L</pubmed_authors><pubmed_authors>Gui J</pubmed_authors><pubmed_authors>Sun X</pubmed_authors><pubmed_authors>Feng S</pubmed_authors><pubmed_authors>Guo A</pubmed_authors><pubmed_authors>Qin B</pubmed_authors><pubmed_authors>Ye J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Umbilical cord blood-derived exosomes attenuate dopaminergic neuron damage of Parkinson's disease mouse model.</name><description>&lt;h4>Background&lt;/h4>Umbilical cord blood (UCB) is a rich source of multifunctional stem cells characterized by low immunogenicity. Recent research in the fields of aging and regenerative medicine has revealed the potential of human umbilical cord blood-derived exosomes (UCB-Exos) in promoting wound healing, anti-aging, and regeneration. However, their role in neurodegenerative diseases, specifically Parkinson's disease (PD), remains unexplored. This study investigates the potential therapeutic effects and underlying mechanisms of UCB-Exos on PD.&lt;h4>Methods&lt;/h4>Large extracellular vesicles (LEv), Exos, and soluble fractions (SF) of human UCB plasma were extracted to investigate their effects on motor dysfunction of the MPTP-induced PD mouse model and identify the key components that improve </description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Sep</publication><modification>2026-06-04T07:26:47.559Z</modification><creation>2025-04-05T18:44:25.389Z</creation></dates><accession>S-EPMC11401276</accession><cross_references><pubmed>39277761</pubmed><doi>10.1186/s12951-024-02773-1</doi></cross_references></HashMap>