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Parkinson Disease: HELP
Articles by Heng Li
Based on 6 articles published since 2010
(Why 6 articles?)
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Between 2010 and 2020, Heng Li wrote the following 6 articles about Parkinson Disease.
 
+ Citations + Abstracts
1 Article The deficiency of NRSF/REST enhances the pro-inflammatory function of astrocytes in a model of Parkinson's disease. 2020

Li, Heng / Liu, Zhaolin / Wu, Yufei / Chen, Yajing / Wang, Jinghui / Wang, Zishan / Huang, Dongping / Wang, Mo / Yu, Mei / Fei, Jian / Huang, Fang. ·The State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Shanghai Medical College, Fudan University; Department of Neurology, Jinan Central Hospital Affiliated to Shandong University, Jinan, China. · The State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Shanghai Medical College, Fudan University. · Department of Neurology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. · School of Life Science and Technology, Tongji University, Shanghai, China; Shanghai Engineering Research Center for Model Organisms, Shanghai Model Organisms Center, INC., Shanghai 201203, China. Electronic address: jfei@tongji.edu.cn. · The State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Shanghai Medical College, Fudan University. Electronic address: huangf@shmu.edu.cn. ·Biochim Biophys Acta Mol Basis Dis · Pubmed #31706914.

ABSTRACT: Neuroinflammation, as an important pathological characteristic of Parkinson's disease (PD), is primarily mediated by activated astrocytes and microglia. Neuron-restrictive silencer factor/repressor element 1 (RE1)-silencing transcription factor (NRSF/REST) regulates many genes and signal pathways involved in the inflammatory process in astrocytes. In the present study, we established the GFAP-Cre:NRSF

2 Article Brain-specific NRSF deficiency aggravates dopaminergic neurodegeneration and impairs neurogenesis in the MPTP mouse model of Parkinson's disease. 2019

Huang, Dongping / Li, Qing / Wang, Yi / Liu, Zhaolin / Wang, Zishan / Li, Heng / Wang, Jinghui / Su, Jing / Ma, Yuanyuan / Yu, Mei / Fei, Jian / Huang, Fang. ·Department of Translational Neuroscience, Jing' an District Centre Hospital of Shanghai, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai 200032, China. · Department of Neurology, Huashan Hospital, Fudan University, Shanghai 200040, China. · School of Life Science and Technology, Tongji University, Shanghai 200092, China. · Shanghai Engineering Research Center for Model Organisms, Shanghai Model Organisms Center, Inc., Shanghai 201203, China. ·Aging (Albany NY) · Pubmed #31147527.

ABSTRACT: Degeneration of the dopaminergic neurons in the substantia nigra and the resultant dopamine depletion from the striatum are the hallmarks of Parkinson's disease (PD) and are responsible for the disease's cardinal motor symptoms. The transcriptional repressor Neuron-Restrictive Silencer Factor (NRSF), also known as RE1-Silencing Transcription Factor (REST), was originally identified as a negative regulator of neuron-specific genes in non-neuronal cells. Our previous study showed that mice deficient in neuronal NRSF/REST expression were more vulnerable to the noxious effects of the dopaminergic neurotoxin MPTP. Here, we found that brain-specific deletion of

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 RESP18 deficiency has protective effects in dopaminergic neurons in an MPTP mouse model of Parkinson's disease. 2018

Su, Jing / Wang, Haoyue / Yang, Yufang / Wang, Jinghui / Li, Heng / Huang, Dongping / Huang, Li / Bai, Xiaochen / Yu, Mei / Fei, Jian / Huang, Fang. ·School of Life Science and Technology, Tongji University, 1239 Siping Road, Shanghai, 200092, China; State Key Laboratory of Medical Neurobiology & Institutes of Brain Science, Fudan University, 138 Yixueyuan Road, Shanghai, 200032, China. Electronic address: 10211010009@fudan.edu.cn. · State Key Laboratory of Medical Neurobiology & Institutes of Brain Science, Fudan University, 138 Yixueyuan Road, Shanghai, 200032, China; Shanghai Research Center for Model Organisms, Pudong, Shanghai, 201203, China. Electronic address: haoyue.wang@shmo.com.cn. · State Key Laboratory of Medical Neurobiology & Institutes of Brain Science, Fudan University, 138 Yixueyuan Road, Shanghai, 200032, China. Electronic address: 13111010009@fudan.edu.cn. · State Key Laboratory of Medical Neurobiology & Institutes of Brain Science, Fudan University, 138 Yixueyuan Road, Shanghai, 200032, China. Electronic address: 15211010011@fudan.edu.cn. · State Key Laboratory of Medical Neurobiology & Institutes of Brain Science, Fudan University, 138 Yixueyuan Road, Shanghai, 200032, China. Electronic address: 13211010006@fudan.edu.cn. · State Key Laboratory of Medical Neurobiology & Institutes of Brain Science, Fudan University, 138 Yixueyuan Road, Shanghai, 200032, China. Electronic address: 12211010008@fudan.edu.cn. · State Key Laboratory of Medical Neurobiology & Institutes of Brain Science, Fudan University, 138 Yixueyuan Road, Shanghai, 200032, China. Electronic address: 15111010011@fudan.edu.cn. · State Key Laboratory of Medical Neurobiology & Institutes of Brain Science, Fudan University, 138 Yixueyuan Road, Shanghai, 200032, China. Electronic address: 13111520001@fudan.edu.cn. · State Key Laboratory of Medical Neurobiology & Institutes of Brain Science, Fudan University, 138 Yixueyuan Road, Shanghai, 200032, China. Electronic address: yumei@fudan.edu.cn. · School of Life Science and Technology, Tongji University, 1239 Siping Road, Shanghai, 200092, China; Shanghai Research Center for Model Organisms, Pudong, Shanghai, 201203, China. Electronic address: jfei@tongji.edu.cn. · State Key Laboratory of Medical Neurobiology & Institutes of Brain Science, Fudan University, 138 Yixueyuan Road, Shanghai, 200032, China. Electronic address: huangf@shmu.edu.cn. ·Neurochem Int · Pubmed #29964075.

ABSTRACT: Regulated endocrine-specific protein, 18 kDa (RESP18) was first cloned in 1994. Its function in the brain especially in neurodegenerative diseases remains unclear. In this study, RESP18 knockout (KO) and littermate wild-type (WT) mice were comprehensively analyzed. The dopaminergic toxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was applied to generate subchronic Parkinson's disease model. We found that KO mice displayed a reduction in locomotor activity and motor coordination under physiological conditions. Five and six days after MPTP administration, the behavioral impairments were detected in MPTP-treated WT mice, whereas such impairments were not detected in MPTP-treated KO mice. The depletion of tyrosine hydroxylase-positive nerve fibers in the striatum was similar between MPTP-treated KO mice and WT littermates. Furthermore, the striatal level of α-synuclein protein was increased by treatment with MPTP in WT mice, but not in KO mice. The loss of dopaminergic neurons was markedly alleviated, and the activation of glial cells was inhibited in the substantia nigra of KO mice challenged with MPTP. These results suggested that RESP18 deficiency might protect dopaminergic neurons against MPTP toxicity.

5 Article Long-term Changes in the Nigrostriatal Pathway in the MPTP Mouse Model of Parkinson's Disease. 2018

Huang, Dongping / Wang, Zishan / Tong, Jiabin / Wang, Mo / Wang, Jinghui / Xu, Jing / Bai, Xiaochen / Li, Heng / Huang, Yulu / Wu, Yufei / Ma, Yuanyuan / Yu, Mei / Huang, Fang. ·The State Key Laboratory of Medical Neurobiology, The Institutes of Brain Science and the Collaborative Innovation Center for Brain Science, School of Basic Medical Sciences, Shanghai Medical College, Fudan University, 138 Yixueyuan Road, Shanghai 200032, China. · School of Life Science and Technology, Tongji University, 1239 Siping Road, Shanghai 200092, China. · School of Basic Medical Sciences, Fudan University, 138 Yixueyuan Road, Shanghai 200032, China. · The State Key Laboratory of Medical Neurobiology, The Institutes of Brain Science and the Collaborative Innovation Center for Brain Science, School of Basic Medical Sciences, Shanghai Medical College, Fudan University, 138 Yixueyuan Road, Shanghai 200032, China. Electronic address: yumei@fudan.edu.cn. · The State Key Laboratory of Medical Neurobiology, The Institutes of Brain Science and the Collaborative Innovation Center for Brain Science, School of Basic Medical Sciences, Shanghai Medical College, Fudan University, 138 Yixueyuan Road, Shanghai 200032, China. Electronic address: huangf@shmu.edu.cn. ·Neuroscience · Pubmed #29196026.

ABSTRACT: Parkinson's disease (PD) is a common and progressive neurodegenerative disorder. The 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD is widely used to study the progression of this disease. Behavior impairment is closely related to the damage of the dopaminergic system in the basal ganglia. Here, MPTP-induced changes in mouse behavior and glial activation were evaluated at different time points after the treatment and the long-term changes in the nigrostriatal pathway were analyzed. We found that mice exposed to MPTP displayed a full recovery in the rotarod test and the pole test but not in the wire hanging test at 65 days post-injection. A biphasic activation of microglial cells was revealed in the nigrostriatal pathway of MPTP-treated mice. However, activation of astrocytes displayed an approximately bell-shaped kinetics and an approximately S-shaped kinetics in the striatum and the substantia nigra, respectively. In addition, the numbers of complement component 3 (C3)-positive neurotoxic astrocytes in the substantia nigra of MPTP-treated mice increased with time and reached a maximum at 42 days, and declined at 74 days, after the treatment. Three months later, the dopaminergic system was partially recovered from the lesion of MPTP. The time course of pathophysiological events has important implications for the interventions or treatment of PD.

6 Article Human cord blood-derived multipotent stem cells (CB-SCs) treated with all-trans-retinoic acid (ATRA) give rise to dopamine neurons. 2012

Li, Xiaohong / Li, Heng / Bi, Jianfen / Chen, Yana / Jain, Sumit / Zhao, Yong. ·Department of Neurology, Jinan Central Hospital, Shandong University, 105 Jiefang Road, Jinan 250013, PR China. ·Biochem Biophys Res Commun · Pubmed #22330803.

ABSTRACT: Parkinson's disease (PD) results from the chronic degeneration of dopaminergic neurons. A replacement for these neurons has the potential to provide a clinical cure and/or lasting treatment for symptoms of the disease. Human cord blood-derived multipotent stem cells (CB-SCs) display embryonic stem cell characteristics, including multi-potential differentiation. To explore their therapeutic potential in PD, we examined whether CB-SCs could be induced to differentiate into dopamine neurons in the presence of all-trans retinoic acid (ATRA). Prior to treatment, CB-SCs expressed mRNA and protein for the key dopaminergic transcription factors Nurr1, Wnt1, and En1. Following treatment with 10 μM ATRA for 12 days, CB-SCs displayed elongated neuronal-like morphologies. Immunocytochemistry revealed that 48 ± 11% of ATRA-treated cells were positive for tyrosine hydroxylase (TH), and 36 ± 9% of cells were positive for dopamine transporter (DAT). In contrast, control CB-SCs (culture medium only) expressed only background levels of TH and DAT. Finally, ATRA-treated CB-SCs challenged with potassium released increased levels of dopamine compared to control. These data demonstrate that ATRA induces differentiation of CB-SCs into dopaminergic neurons. This finding may lead to the development of an alternative approach to stem cell therapy for Parkinson's disease.