The dysregulated Pink1 mitochondrial proteome is partially corrected with exercise
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Updated: Nov 3, 2025

Measurement of Oxygen Consumption Rate in Acute Striatal Slices from Adult Mice
Published on: June 8, 2022
Brad Ebanks1, Thomas L Ingram1, Gunjan Katyal1
1School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, LE12 5RD, UK.
Abstract:
One of the genes which has been linked to the onset of juvenile/early onset Parkinson's disease (PD) is PINK1. There is evidence that supports the therapeutic potential of exercise in the alleviation of PD symptoms. It is possible that exercise may enhance synaptic plasticity, protect against neuro-inflammation and modulate L-Dopa regulated signalling pathways. We explored the effects of exercise on Pink1 deficient Drosophila melanogaster which undergo neurodegeneration and muscle degeneration. We used a 'power-tower' type exercise platform to deliver exercise activity to Pink1 and age matched wild-type Drosophila. Mitochondrial proteomic profiles responding to exercise were obtained. Of the 516 proteins identified, 105 proteins had different levels between Pink1 and wild-type non-exercised Drosophila. Gene ontology enrichment analysis and STRING network analysis highlighted proteins and pathways with altered expression within the mitochondrial proteome. Comparison of the Pink1 exercised proteome to wild-type proteomes showed that exercising the Pink1 caused their proteomic profile to return towards wild-type levels.
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