A Disruption Mechanism of the Molecular Clock in a MPTP Mouse Model of Parkinson’s Disease
作者： Akane Hayashi , Naoya Matsunaga , Hiroyuki Okazaki , Keisuke Kakimoto , Yoshinori Kimura
DOI: 10.1007/S12017-012-8214-X
关键词:
摘要: Parkinson’s disease (PD) is a common neurodegenerative disorder that characterized by the degeneration of dopaminergic neurons in substantia nigra and dopamine depletion striatum. Although motor symptoms are still regarded as main problem, non-motor PD also markedly impair quality life. Several symptoms, such sleep disturbances depression, suggested to be implicated alteration circadian clock function. In this study, we investigated disruption mechanism 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model PD. MPTP-treated mice exhibited altered 24-h rhythms body temperature locomotor activity. addition, MPTP treatment affected system at genetic level. The exposure human neuroblastoma cells (SH-SY5Y) 1-metyl-4-phenylpyridinium (MPP+) increased or decreased mRNA levels several genes dose-dependent manner. MPP+-induced changes expression were reversed Compound C, an inhibitor AMP-activated protein kinase (AMPK). Most importantly, addition ATP drinking water attenuated neurodegeneration neurons, suppressed AMPK activation prevented disruption. present findings suggest caused dysfunction, may novel therapeutic strategy based on molecular
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