mTOR Signaling in Parkinson’s Disease
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As a key regulator of cell metabolism and survival, mechanistic target of rapamycin (mTOR) emerges as a novel therapeutic target for Parkinson’s disease (PD). A growing body of research indicates that restoring perturbed mTOR signaling in PD models can prevent neuronal cell death. Nevertheless, molecular mechanisms underlying mTOR-mediated effects in PD have not been fully understood yet. Here, we review recent progress in characterizing the association of mTOR signaling with PD risk factors and further discuss the potential roles of mTOR in PD.
KeywordsmTOR Parkinson’s disease Apoptosis α-Synuclein Oxidative stress
The authors gratefully acknowledge the financial support from the National Natural Science Foundation of China (Grant No. 11375213, 21390411) and Hundred Talents Program of the Chinese Academy of Sciences.
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Conflict of interest
The authors declare that they have no conflict of interest.
- Decressac, M., & Bjorklund, A. (2013). mTOR inhibition alleviates L-DOPA-induced dyskinesia in parkinsonian rats. Journal of Parkinsons Disease, 3, 13–17.Google Scholar
- Jiang, T. F., et al. (2013b). Curcumin ameliorates the neurodegenerative pathology in A53T α-synuclein cell model of Parkinson’s disease through the downregulation of mTOR/p70S6K signaling and the recovery of macroautophagy. Journal of Neuroimmune Pharmacology, 8, 356–369.PubMedCrossRefGoogle Scholar
- Lin, X., et al. (2012). Conditional expression of Parkinson’s disease-related mutant a-synuclein in the midbrain dopaminergic neurons causes progressive neurodegeneration and degradation of transcription factor nuclear receptor related 1. Journal of Neuroscience, 32, 9248–9264.PubMedPubMedCentralCrossRefGoogle Scholar
- Tee, A. R., et al. (2002). Tuberous sclerosis complex-1 and -2 gene products function together to inhibit mammalian target of rapamycin (mTOR)-mediated downstream signaling. Proceedings of the National Academy of Sciences of the United States of America, 99, 13571–13576.PubMedPubMedCentralCrossRefGoogle Scholar