A GSK3α/β and CDKs inhibitor improves mitochondrial function in human neurons

Gongyu Shi, Helen L Scott, Nur Izzah Farhana B Mohamad Azhar, Andriana Gialeli, Oscar Cordero Llana, James B Uney*

*Corresponding author for this work

Research output: Contribution to conferenceConference Posterpeer-review


Parkinson’s is a progressively debilitating neurodegenerative condition that occurs primarily in old age. As a result of the global population increase in longevity, there is also an increase in the incidence of PD.1. 2 A significant amount of knowledge has been gathered regarding the biochemical and genetic changes that underpin the clinical manifestation. However, there is still no cure for Parkinson’s. Our understanding of the molecular mechanisms that cause familial Parkinson’s has been increased by identifying mutations in genes (SNCA, LRRK2, PARK7, PINK1, and PRKN). In addition, environmental toxins such as rotenone and MPP+ can cause Parkinson’s like syndromes. Mitochondrial dysfunction has been found in studies of both familial and sporadic forms. For instance, the familial genes PINK1 and PRKN play crucial roles in mitochondrial quality control. Hence, to identify neuroprotective drugs, studies have attempted to identify drugs that improve mitochondrial health. Here we aim to identify the best-repurposed kinase inhibitor that rescues pathological phenotypes in a mitochondrial dysfunction model of Parkinson’s.
Original languageEnglish
Publication statusPublished - Sept 2022
EventEMBO / FEBS: Mitochondria in life, death and disease - Budva, Montenegro
Duration: 27 Sept 20221 Nov 2022


ConferenceEMBO / FEBS
Internet address


  • Parkinson Disease
  • Mitochondria
  • GSK-3β
  • Drug Screening


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