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

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.