English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Parkinson's disease (PD) is the second most common neurodegenerative disease in middle-aged and elderly people. However, the etiology and pathogenesis of PD are still unclear and there is a lack of reliable biomarkers for early molecular diagnosis. Parkin (encoded by  PARK2 ) is a ubiquitin E3 ligase that participates in mitochondrial homeostasis, the ubiquitin-proteasome pathway, oxidative stress response, and cell death pathways, which are involved in the pathogenesis of PD. However, Parkin is also expressed in peripheral blood lymphocytes (PBLs). In this study, permanent lymphocyte lines were established from the peripheral blood of sporadic PD (sPD) patients,  PARK2  mutation carriers, and healthy controls. Reactive oxygen species (ROS), function of the mitochondrial respiratory chain complex I, and apoptosis were analyzed in the PBLs. There was no significant difference in ROS, mitochondrial respiratory chain complex I, and apoptosis between the experimental groups and the control group without paraquat treatment. Compared with the control group of healthy subjects, we found an increase of ROS (control 100 ± 0, sPD 275.53 ± 79.11, and C441R 340 ± 99.67) and apoptosis, as well as a decline in the function of mitochondrial respiratory chain complex I in PBLs of  PARK2  mutation carriers and sPD after the treatment of paraquat (control 0.65 ± 0.08, sPD 0.44 ± 0.08, and C441R 0.32 ± 0.08). Moreover, overexpression of the wild-type (WT)  PARK2  in HeLa cells and immortalized PBLs could rescue mitochondrial function and partially inhibit apoptosis following paraquat treatment, while the C441R mutation could not. Thus, ROS levels, activity of mitochondrial respiratory chain complex I, and apoptosis of PBLs are potential diagnostic biomarkers of PD.

The PARK2 Mutation Associated with Parkinson’s Disease Enhances the Vulnerability of Peripheral Blood Lymphocytes to Paraquat