Deficiency of leads to accelerated aging and neuroprotection in MPTP-induced Parkinson's disease mice.

Studies reveal a linkage of miR-29s in aging and Parkinson's disease (PD). Here we show that the serum levels of miR-29s in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mice exhibited dynamic changes. The role of in aging and PD was studied utilizing gene knockout mice ( KO). KO mice were characterized by a markedly lighter weight, kyphosis, muscle weakness and abnormal gait, when compared with wild-type (WT) mice. The WT also developed apparent dermis thickening and adipose tissue reduction. However, deficiency of alleviated MPTP-induced damages of the dopaminergic system and glial activation in the nigrostriatal pathway and consequently improved the motor function of MPTP-treated KO mice. Knockout of inhibited the expression of inflammatory factors in 1-methyl-4-phenylpyridinium (MPP)-treated primary cultures of mixed glia, primary astrocytes, or LPS-treated primary microglia. Moreover, deficiency enhanced the activity of AMPK but repressed the NF-κB p65 signaling in glial cells. Our results show that KO mice display the progeria-like phenotype. Less activated glial cells and repressed neuroinflammation might bring forth dopaminergic neuroprotection in KO mice. Conclusively, is involved in the regulation of aging and plays a detrimental role in Parkinson's disease.