Amelioration of pathologic α-synuclein-induced Parkinson's disease by irisin.
Tae-In KamHyejin ParkShih-Ching ChouJonathan G Van VrankenMelanie J MittenbühlerHyeonwoo KimMu AYu Ree ChoiDevanik BiswasJustin WangYu ShinAlexis LoderSenthilkumar S KaruppagounderChristiane D WrannValina L DawsonBruce M SpiegelmanTed M DawsonPublished in: Proceedings of the National Academy of Sciences of the United States of America (2022)
Physical activity provides clinical benefit in Parkinson's disease (PD). Irisin is an exercise-induced polypeptide secreted by skeletal muscle that crosses the blood-brain barrier and mediates certain effects of exercise. Here, we show that irisin prevents pathologic α-synuclein (α-syn)-induced neurodegeneration in the α-syn preformed fibril (PFF) mouse model of sporadic PD. Intravenous delivery of irisin via viral vectors following the stereotaxic intrastriatal injection of α-syn PFF cause a reduction in the formation of pathologic α-syn and prevented the loss of dopamine neurons and lowering of striatal dopamine. Irisin also substantially reduced the α-syn PFF-induced motor deficits as assessed behaviorally by the pole and grip strength test. Recombinant sustained irisin treatment of primary cortical neurons attenuated α-syn PFF toxicity by reducing the formation of phosphorylated serine 129 of α-syn and neuronal cell death. Tandem mass spectrometry and biochemical analysis revealed that irisin reduced pathologic α-syn by enhancing endolysosomal degradation of pathologic α-syn. Our findings highlight the potential for therapeutic disease modification of irisin in PD.
Keyphrases
- neoadjuvant chemotherapy
- cell death
- physical activity
- skeletal muscle
- high glucose
- mouse model
- tandem mass spectrometry
- diabetic rats
- locally advanced
- high performance liquid chromatography
- drug induced
- endothelial cells
- high resolution
- insulin resistance
- sars cov
- radiation therapy
- signaling pathway
- metabolic syndrome
- low dose
- simultaneous determination
- body composition
- risk assessment
- rectal cancer
- late onset
- cell proliferation
- subarachnoid hemorrhage
- stress induced
- protein kinase