ADP/ATP translocase 1 protects against an α-synuclein-associated neuronal cell damage in Parkinson’s disease model

Abstract Background ADP/ATP translocase 1 (ANT1) is involved in the exchange of cytosolic ADP and mitochondrial ATP, its defection plays an important role pathogenesis. To reveal etiological implication ANT1 for Parkinson’s disease (PD), a neurodegenerative disorder, mouse model treated with 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine neuroblastoma cell induced by 1-methyl-4-pehny1-pyridine were utilized this study. Results The tissue-specific abundance brains was accessed using analysis Western blot immunohistochemistry. Down-regulated soluble found to be correlated PD, associated PD pathogenesis via forming protein aggregates α-synuclein. This finding confirmed at cellular level models. supplement neuronal cells revealed protective roles against cytotoxicity caused MPP + . Protein interaction assay, coupled LC-MS/MS, silver-stained SDS-PAGE anti-ANT1 antibody respectively, illustrated α-synuclein expressed as bite. Additionally, significant increasing ROSs detected -treated cells. Conclusions study indicated that potentially causative factor led neuropathogenic injury promoting formation investigation promotes innovative understanding on etiology provides valuable information developing potential drug targets treatment or reliable biomarkers prognostication.