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Parkinson Disease: HELP
Articles by Ya Feng
Based on 5 articles published since 2010
(Why 5 articles?)
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Between 2010 and 2020, Ya Feng wrote the following 5 articles about Parkinson Disease.
 
+ Citations + Abstracts
1 Review Epigenetic mechanisms in Parkinson's disease. 2015

Feng, Ya / Jankovic, Joseph / Wu, Yun-Cheng. ·Department of Neurology, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, PR China. · Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, TX 77030, USA. · Department of Neurology, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, PR China. Electronic address: yunchw@medmail.com.cn. ·J Neurol Sci · Pubmed #25553963.

ABSTRACT: Parkinson's disease (PD) is the second most common age-related neurodegenerative disease, but its pathogenesis is not fully understood. The selective neuronal cell death in PD has been considered to result from a complex interaction between genetic and environmental factors, but the nature of the relationship between the two chief modifiers remains to be elucidated. There is a growing body of evidence supporting the role of epigenetics in the development and progression of many neurodegenerative diseases including PD. Epigenetic modification refers to changes in gene expression or function without changes in DNA sequence, which mainly includes DNA methylation, post-modifications of histone, and non-coding RNAs. In this review, we will focus on the abnormal epigenetic modifications involved in the pathogenesis of PD and their implications for the development of future diagnostic and therapeutic strategies.

2 Article Resveratrol alleviates MPTP-induced motor impairments and pathological changes by autophagic degradation of α-synuclein via SIRT1-deacetylated LC3. 2016

Guo, Yan-Jie / Dong, Su-Yan / Cui, Xin-Xin / Feng, Ya / Liu, Te / Yin, Ming / Kuo, Sheng-Han / Tan, Eng-King / Zhao, Wen-Juan / Wu, Yun-Cheng. ·Department of Neurology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, P.R. China. · Shanghai Geriatric Institute of Chinese Medicine, Longhua Hospital, , Shanghai University of Traditional Chinese Medicine, Shanghai, P.R. China. · School of Pharmacy, Shanghai Jiao Tong University, Shanghai, P.R. China. · Department of Neurology, College of Physicians and Surgeons, Columbia University, NY, USA. · Department of Neurology, Singapore General Hospital, National Neuroscience Institute, Singapore. · Department of Neurology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, P.R. China. yunchw@medmail.com.cn. ·Mol Nutr Food Res · Pubmed #27296520.

ABSTRACT: SCOPE: The accumulation of misfolded α-synuclein in dopaminergic neurons is the leading cause of Parkinson's disease (PD). Resveratrol (RV), a polyphenolic compound derived from grapes and red wine, exerts a wide range of beneficial effects via activation of sirtuin 1 (SIRT1) and induction of vitagenes. Here, we assessed the role of RV in a 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) induced mouse model of PD and explored its potential mechanisms. METHODS AND RESULTS: RV and EX527, a specific inhibitor of SIRT1, were administered before and after MPTP treatment. RV protected against MPTP-induced loss of dopaminergic neurons, and decreases in tyrosine hydroxylase and dopamine levels, as well as behavioral impairments. Meanwhile, RV administration activated SIRT1. Microtubule-associated protein 1 light chain 3 (LC3) was then deacetylated and redistributed from the nucleus to the cytoplasm, which provoked the autophagic degradation of α-synuclein in dopaminergic neurons. Furthermore, EX527 antagonized the neuroprotective effects of RV by reducing LC3 deacetylation and subsequent autophagic degradation of α-synuclein. CONCLUSION: We showed that RV ameliorated both motor deficits and pathological changes in MPTP-treated mice via activation of SIRT1 and subsequent LC3 deacetylation-mediated autophagic degradation of α-synuclein. Our observations suggest that RV may be a potential prophylactic and/or therapeutic agent for PD.

3 Article The epigenetic regulation of HIF-1α by SIRT1 in MPP(+) treated SH-SY5Y cells. 2016

Dong, Su-Yan / Guo, Yan-Jie / Feng, Ya / Cui, Xin-Xin / Kuo, Sheng-Han / Liu, Te / Wu, Yun-Cheng. ·Department of Neurology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, PR China. · Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, USA. · Shanghai Geriatric Institute of Chinese Medicine, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200031, PR China. Electronic address: liute1979@126.com. · Department of Neurology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, PR China. Electronic address: yunchw@medmail.com.cn. ·Biochem Biophys Res Commun · Pubmed #26768367.

ABSTRACT: Both silent information regulator 1 (SIRT1) and hypoxia inducible factor 1 (HIF-1) have been found to play important roles in the pathophysiology of Parkinson's disease (PD). However, their mechanisms and their relationship still require further study. In the present study, we focused on the change and relationship of SIRT1 and HIF-1α in PD. PD cell models were established by using methyl-4-phenylpyridinium (MPP(+)), which induced inhibition of cell proliferation, cell cycle arrest and apoptosis. We found that the expression of HIF-1α and its target genes VEGFA and LDHA increased and that SIRT1 expression was inhibited in MPP(+) treated cells. With further analysis, we found that the acetylation of H3K14 combined with the HIF-1α promoter was dramatically increased in cells treated with MPP(+), which resulted in the transcriptional activation of HIF-1α. Moreover, the acetylation of H3K14 and the expression of HIF-1α increased when SIRT1 was knocked down, suggesting that SIRT1 was involved in the epigenetic regulation of HIF-1α. At last, phenformin, another mitochondrial complex1 inhibitor, was used to testify that the increased HIF-1a was not due to off target effects of MPP(+). Therefore, our results support a link between PD and SIRT1/HIF-1α signaling, which may serve as a clue for understanding PD.

4 Article Clinical characteristics of leg restlessness in Parkinson's disease compared with idiopathic Restless Legs Syndrome. 2015

Zhu, Xiao-Ying / Liu, Ye / Zhang, Xiao-Jin / Yang, Wen-Hao / Feng, Ya / Ondo, William G / Tan, Eng-King / Wu, Yun-Cheng. ·Department of Neurology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, PR China. · Department of Neurology, University of Texas Health Science Center Houston, Houston, TX, USA. · Department of Neurology, Singapore General Hospital, National Neuroscience Institute, Outram Road, Singapore. · Department of Neurology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, PR China. Electronic address: yunchw@medmail.com.cn. ·J Neurol Sci · Pubmed #26189051.

ABSTRACT: OBJECTIVE: There is limited data on motor restlessness in Parkinson's disease (PD). Here we evaluate for clinical differences between cohorts of idiopathic Restless Legs Syndrome (iRLS), PD patients with leg restlessness, and PD with RLS. METHODS: We examined 276 consecutive PD patients for leg restlessness symptoms, we compared clinical features of PD patients with RLS, PD patients with leg restlessness but not meeting RLS criteria, PD patient without RLS and iRLS. RESULTS: A total of 262 PD patients who satisfied the inclusion criteria were analyzed. After excluding 23 possible secondary RLS or mimics, 28 were diagnosed with RLS and 18 with leg motor restlessness (LMR). Compared with iRLS patients, PD patients with RLS or LMR had older age of RLS/LMR onset, shorter duration of leg restlessness, less positive family history, different seasonal trends and more unilaterality of leg restlessness symptom (P<0.01) which were often in accordance with dominant Parkinsonism side and related with Parkinsonism severity. PD patients with RLS/LMR had lower daily dosage (P<0.01) and shorter duration (P<0.05) of dopaminergic medication when RLS/LMR symptom onset than PD without leg restlessness. PD with LMR had less severe Parkinsonism (P<0.05) and leg restlessness (P<0.01) symptoms than PD with RLS. CONCLUSION: Clinical characteristics of PD patients with RLS and LMR were different from iRLS, differentiating these various subtypes can facilitate optimal treatment.

5 Article Neuroprotection by Orexin-A via HIF-1α induction in a cellular model of Parkinson's disease. 2014

Feng, Ya / Liu, Te / Li, Xin-Qun / Liu, Ye / Zhu, Xiao-Ying / Jankovic, Joseph / Pan, Tian-Hong / Wu, Yun-Cheng. ·Department of Neurology, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, PR China. · Shanghai Geriatric Institute of Chinese Medicine, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200031, PR China. · Department of Experimental Therapeutics, M.D. Anderson Cancer Center, Houston, TX 77030, USA. · Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, TX 77030, USA. · Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, TX 77030, USA. Electronic address: Tpan1@mdanderson.org. · Department of Neurology, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, PR China. Electronic address: yunchw@medmail.com.cn. ·Neurosci Lett · Pubmed #25038418.

ABSTRACT: Orexin-A, a neuropeptide secreted by hypothalamic neurons, may be neuroprotective in many neurological conditions such as cerebral ischaemia. One mechanism postulated to be involved in the neuroprotection by Orexin-A is the induction of hypoxia inducible factor 1 alpha (HIF-1α). Parkinson's disease (PD) is a progressive neurodegenerative disorder and mitochondrial dysfunction has been demonstrated to play a role in its pathogenesis. Mitochondrial dysfunction may cause reduction of O2 consumption and subsequently activate prolyl hydroxylase, which leads to decreased level of HIF-1α. In this study, we used MPP(+)-treated SH-SY5Y cells as an in vitro cellular model of PD to test the role of Orexin-A as an inducer of HIF-1α. Our results showed that Orexin-A not only induced HIF-1α but also activated downstream targets of HIF-1α, such as vascular endothelial growth factor and erythropoietin. Thus, Orexin-A treatment attenuated MPP(+)-induced cell injury and this effect was blocked when HIF-1α was suppressed. Hence, we conclude that induction of HIF-1α is one of the mechanisms involved in the neuroprotection by Orexin-A.