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Parkinson Disease: HELP
Articles by Yun-Cheng Wu
Based on 11 articles published since 2010
(Why 11 articles?)
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Between 2010 and 2020, Yuncheng Wu wrote the following 11 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 Review Preclinical biomarkers of Parkinson disease. 2011

Wu, Yuncheng / Le, Weidong / Jankovic, Joseph. ·Department of Neurology, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. ·Arch Neurol · Pubmed #21220674.

ABSTRACT: The search for markers of preclinical Parkinson disease (PD) is becoming increasingly important because pathogenesis-targeted neuroprotective strategies are being developed for future use in at-risk populations, even before clinical onset of disease. Advances in clinical recognition of early symptoms and signs, development of new neuroimaging probes and technologies, identification of new neuropathological markers of PD, and breakthroughs in genetics and basic neuroscience are gradually translating into better understanding of predisposing and preclinical factors that lead to progressive neurodegeneration. Coupled with system biology tools, progress is being made in the identification of new genomic, transcriptomic, proteomic, lipidomic, and metabolomic molecules and new signaling pathways that are relevant to the pathogenesis of neurodegeneration in PD. These new tools will be critical not only in the discovery of sensitive, specific, and reliable biomarkers of preclinical PD but also in the development of tests that will aid in the early detection and differential diagnosis of parkinsonian disorders and in monitoring disease progression.

3 Article Dl-3- 2019

Chen, Yajing / Wu, Tingting / Li, Heng / Li, Xuan / Li, Qing / Zhu, Xiaoying / Yu, Mei / Kuo, Sheng-Han / Huang, Fang / Wu, Yun-Cheng. ·Department of Neurology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. · Department of Neurology, Jinan Central Hospital Affiliated to Shandong University, Jinan, China. · The State Key Laboratory of Medical Neurobiology, The Institutes of Brain Science and the Collaborative Innovation Center for Brain Science, Shanghai Medical College, Fudan University, Shanghai, China. · Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, NY, United States. ·Front Aging Neurosci · Pubmed #30873019.

ABSTRACT: Microglia-mediated neuroinflammation contributes to multiple neurodegenerative disorders, including PD. Therefore, the regulation of microglial activation probably has the therapeutic potential. This study is aimed to determine whether NBP could suppress microglial activation and protect dopaminergic neurons from excessive neuroinflammation. In the present study, MPTP-induced PD model was established to explore the neuroprotective and anti-inflammatory effect of NBP. We assessed motor deficits, dopaminergic neurodegeneration and microglial activation in PD mice.

4 Article Therapeutic Potential of a Prolyl Hydroxylase Inhibitor FG-4592 for Parkinson's Diseases 2018

Li, Xuan / Cui, Xin-Xin / Chen, Ya-Jing / Wu, Ting-Ting / Xu, Huaxi / Yin, Huiyong / Wu, Yun-Cheng. ·Department of Neurology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. · Neuroscience Initiative, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA, United States. · Key Laboratory of Food Safety Research, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China. · Key Laboratory of Food Safety Risk Assessment, Ministry of Health, Beijing, China. · School of Life Sciences and Technology, ShanghaiTech University, Shanghai, China. ·Front Aging Neurosci · Pubmed #29755339.

ABSTRACT: As the main transcription factor that regulates the cellular responses to hypoxia, Hypoxia-inducible factor-1α (HIF-1α) plays an important role in the pathogenesis of Parkinson's disease (PD). HIF-1α is normally degraded through ubiquitination after hydroxylation by prolyl hydroxylases (PHD). Emerging evidence has suggested that HIF PHD inhibitors (HIF-PHI) may have neuroprotective effects on PD through increasing HIF-1α levels. However, the therapeutic benefit of HIF-PHI for PD remains poorly explored due to the lack of proper clinical compounds and understanding of the underlying molecular mechanisms. In this study, we examined the therapeutic benefit of a new HIF-PHI, FG-4592, which is currently in phase 3 clinical trials to treat anemia in patients with chronic kidney diseases (CKD) in PD models. FG-4592 attenuates MPP

5 Article Clinical features of Parkinson's disease with and without rapid eye movement sleep behavior disorder. 2017

Liu, Ye / Zhu, Xiao-Ying / Zhang, Xiao-Jin / Kuo, Sheng-Han / Ondo, William G / Wu, Yun-Cheng. ·Department of Neurology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, No.100, Haining Road, Shanghai, 200080 People's Republic of China. · Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, USA. · 0000000419368729 · grid.21729.3f · Methodist Neurological Institute, Houston, TX USA. · 000000041936877X · grid.5386.8 ·Transl Neurodegener · Pubmed #29296278.

ABSTRACT: Background: Rapid eye movement sleep behavior disorder (RBD) and Parkinson's disease (PD) are two distinct clinical diseases but they share some common pathological and anatomical characteristics. This study aims to confirm the clinical features of RBD in Chinese PD patients. Methods: One hundred fifty PD patients were enrolled from the Parkinson`s disease and Movement Disorders Center in  Department of Neurology, Shanghai General Hospital from January 2013 to August 2014. This study examined PD patients with or without RBD as determined by the REM Sleep Behavior Disorder Screening Questionnaire (RBDSQ), assessed motor subtype by Unified PD Rating Scale (UPDRS) III at "on" state, and compared the sub-scale scores representing tremor, rigidity, appendicular and axial. Investigators also assessed the Hamilton Anxiety Scale (HAMA), Hamilton Depression Scale (HAMD), Mini-Mental State Examination (MMSE), Clinical Dementia Rating (CDR), and Parkinson's disease Sleep Scale (PDSS). Results: One hundred fourty one PD patients entered the final study. 30 (21.28%) PD patients had probable RBD (pRBD) diagnosed with a RBDSQ score of 6 or above. There were no significant differences for age, including age of PD onset and PD duration, gender, smoking status, alcohol or coffee use, presence of anosmia or freezing, UPDRS III, and H-Y stages between the pRBD Conclusion: pRBD

6 Article SIRT3 deacetylated and increased citrate synthase activity in PD model. 2017

Cui, Xin-Xin / Li, Xuan / Dong, Su-Yan / Guo, Yan-Jie / 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, The Third Affiliated Hospital of Xinxiang Medical University, Xinxiang, 453003, PR China. · Shanghai Geriatric Institute of Chinese Medicine, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, 200031, PR China. Electronic address: teliu79@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 #28161643.

ABSTRACT: SIRT3 have been found to be neuroprotective in many neurological diseases, but its detail mechanism is only partially understood. In this study, MPP

7 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.

8 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.

9 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.

10 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.

11 Article Effects of deep brain stimulation in relatively young-onset multiple system atrophy Parkinsonism. 2014

Zhu, Xiao-Ying / Pan, Tian-Hong / Ondo, William G / Jimenez-Shahed, Joohi / 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 Disorder Clinic, Department of Neurology, Baylor College of Medicine, Houston 77030, TX, USA. · Department of Neurology, University of Texas Health Science Center Houston, Houston, TX, 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 #24831987.

ABSTRACT: OBJECTIVE: The aim of this study was to analyze outcomes after 1 year of bilateral STN deep brain stimulation (DBS) in relatively young-onset patients with multiple system atrophy-Parkinsonism (MSA-P). BACKGROUND: The efficacy of DBS has been demonstrated in idiopathic Parkinson's disease. However, the experience with DBS in relatively young-onset MSA-P is limited and controversial. METHODS: Information about the demographic and clinical data from five MSA patients treated with STN DBS was entered into a database and analyzed. RESULTS: Five patients with relatively young-onset MSA (mean age at onset 42.2±2.2 years, 3 women, 2 men) have been treated with bilateral STN stimulators, the mean duration between DBS surgery and disease onset was 7.0±3.5 years. All of the patients had dyskinesia and postural instability, and subjective benefit from levodopa. During the 6 months after surgery, the clinical status of three patients improved with a decrease of dyskinesia. However, by 1 year, the symptoms reappeared and progressed in all patients. Overall, the mean "off" medication UPDRS-III score worsened 23.5±15.3 1 year after surgery and the levodopa dosage was not reduced. CONCLUSIONS: This data does not support the use of STN DBS for relatively young-onset MSA-P.