Just like a car needing a jumpstart, exercise can reinvigorate the brain circuits affected by Parkinson’s disease (PD). Scientists conducted a study on a PD mouse model and found that 12 weeks of treadmill exercise significantly improved motor symptoms. By analyzing RNA sequences of different brain regions, they discovered that the substantia nigra and striatum showed the most notable changes in response to exercise. These regions exhibited upregulation of genes involved in synaptic regulation pathways essential for axon guidance, synapse assembly, neurogenesis, and more. Additionally, immunofluorescence staining confirmed that exercise helped preserve TH+ synapses in the striatum, reinforcing the protective effects. This research sheds light on the specific brain regions and molecular pathways influenced by exercise in PD. It suggests that exercise-induced changes in synaptic regulation play a crucial role in countering the effects of the disease. To dive deeper into the study findings, check out the full article.
BackgroundExercise plays an essential role in improving motor symptoms in Parkinson’s disease (PD), but the underlying mechanism in the central nervous system remains unclear.MethodsMotor ability was observed after 12-week treadmill exercise on a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mouse model of PD. RNA-sequencing on four brain regions (cerebellum, cortex, substantia nigra (SN), and striatum) from control animals, MPTP-induced PD, and MPTP-induced PD model treated with exercise for 12 weeks were performed. Transcriptional networks on the four regions were further identified by an integrative network biology approach.ResultsThe 12-week treadmill exercise significantly improved the motor ability of an MPTP-induced mouse model of PD. RNA-seq analysis showed SN and striatum were remarkably different among individual region’s response to exercise in the PD model. Especially, synaptic regulation pathways about axon guidance, synapse assembly, neurogenesis, synaptogenesis, transmitter transport-related pathway, and synaptic regulation genes, including Neurod2, Rtn4rl2, and Cd5, were upregulated in SN and striatum. Lastly, immunofluorescence staining revealed that exercise rescued the loss of TH+ synapses in the striatal region in PD mice, which validates the key role of synaptic regulation pathways in exercise-induced protective effects in vivo.ConclusionSN and striatum are important brain regions in which critical transcriptional changes, such as in synaptic regulation pathways, occur after the exercise intervention on the PD model.
Dr. David Lowemann, M.Sc, Ph.D., is a co-founder of the Institute for the Future of Human Potential, where he leads the charge in pioneering Self-Enhancement Science for the Success of Society. With a keen interest in exploring the untapped potential of the human mind, Dr. Lowemann has dedicated his career to pushing the boundaries of human capabilities and understanding.
Armed with a Master of Science degree and a Ph.D. in his field, Dr. Lowemann has consistently been at the forefront of research and innovation, delving into ways to optimize human performance, cognition, and overall well-being. His work at the Institute revolves around a profound commitment to harnessing cutting-edge science and technology to help individuals lead more fulfilling and intelligent lives.
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