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Parkinson Disease: HELP
Articles by Yan Chen
Based on 12 articles published since 2010
(Why 12 articles?)
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Between 2010 and 2020, Yan Chen wrote the following 12 articles about Parkinson Disease.
 
+ Citations + Abstracts
1 Review Genetics of Parkinson's disease and related disorders. 2018

Zhang, Pei-Lan / Chen, Yan / Zhang, Chen-Hao / Wang, Yu-Xin / Fernandez-Funez, Pedro. ·Department of Neurology, Tianjin Huanhu Hospital, Tianjin, China. · Department of Biomedical Sciences, University of Minnesota Medical School-Duluth Campus, Duluth, Minnesota, USA. ·J Med Genet · Pubmed #29151060.

ABSTRACT: Parkinson's disease (PD) is a complex and heterogeneous neurological condition characterised mainly by bradykinesia, resting tremor, rigidity and postural instability, symptoms that together comprise the parkinsonian syndrome. Non-motor symptoms preceding and following clinical onset are also helpful diagnostic markers revealing a widespread and progressive pathology. Many other neurological conditions also include parkinsonism as primary or secondary symptom, confounding their diagnosis and treatment. Although overall disease course and end-stage pathological examination single out these conditions, the significant overlaps suggest that they are part of a continuous disease spectrum. Recent genetic discoveries support this idea because mutations in a few genes (α-synuclein,

2 Article Thyroid hormone levels and structural parameters of thyroid homeostasis are correlated with motor subtype and disease severity in euthyroid patients with Parkinson's disease. 2020

Tan, Yinyin / Gao, Lei / Yin, Qingqing / Sun, Zhanfang / Man, Xiao / Du, Yifeng / Chen, Yan. ·Department of Neurology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, Shandong, China; · Department of Neurology, The People Hospital of Huaiyin, Jinan 250021, Shandong, China; · Department of Geriatrics, Department of Geriatric Neurology, Shandong Provincial Hospital, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan 250021, Shandong, China. ·Int J Neurosci · Pubmed #32186220.

ABSTRACT:

3 Article Astragalus polysaccharide exerts anti-Parkinson via activating the PI3K/AKT/mTOR pathway to increase cellular autophagy level in vitro. 2020

Tan, Yinyin / Yin, Ling / Sun, Zhanfang / Shao, Shanshan / Chen, Wenbin / Man, Xiao / Du, Yifeng / Chen, Yan. ·Department of Neurology, Shandong Provincial Hospital affiliated to Shandong University, Jinan, Shandong 250021, China. · Department of Endocrinology, Shandong Provincial Hospital affiliated to Shandong University, Jinan, Shandong 250021, China. · Scientific Center, Shandong Provincial Hospital affiliated to Shandong First Medical University, Jinan, Shandong 250021, China; Shandong Provincial Key Laboratory of Endocrinology and Lipid Metabolism, Jinan, Shandong 250021, China. · Department of Neurology, Shandong Provincial Hospital affiliated to Shandong University, Jinan, Shandong 250021, China. Electronic address: cyrz001@163.com. ·Int J Biol Macromol · Pubmed #32112840.

ABSTRACT: Astragalus polysaccharide (APS) is a bioactive macromolecule, which has been used to alleviate the development of Parkinson's disease (PD), while its mechanism is still unresolved. As is generally accepted that autophagy has an important link with PD, thus it is reasonable to hypothesize that APS was involved in autophagy pathway for the presence of anti-PD. To verify this hypothesis, PD model was induced by 100 μM 6-hydroxydopamine (6-HODA) in PC12 cells and then treated with different concentration of APS. Results showed that APS could increase cell viability and the level of autophagy, improve the formation of autophagosome, promote the conversion of LC3-I to LC3-II, showing APS could improve autophagy level. Moreover, APS could down-regulate the expression of pAKT and pmTOR, and up-regulate the expression of PTEN. While these proteins are involved in PI3K/AKT/mTOR pathway, we then knocked down (KD) endogenous PI3K protein (the PI3K/AKT/mTOR pathway receptor protein) in PC12 cells. Results showed that these events regulated by APS were reversed in PI3K KD cells, shown that APS activated autophagy through PI3K/AKT/mTOR pathway for treating PD. Altogether, APS has the role of increasing autophagy, and this event was responsible for inhibiting PI3K protein to activate PI3K/AKT/mTOR pathway.

4 Article 5-Substituted-N-pyridazinylbenzamides as potent and selective LRRK2 inhibitors: Improved brain unbound fraction enables efficacy. 2019

Ding, Xiao / Stasi, Luigi Piero / Dai, Xuedong / Long, Kai / Peng, Cheng / Zhao, Baowei / Wang, Hailong / Sun, Changhui / Hu, Huan / Wan, Zehong / Jandu, Karamjit S / Philps, Oliver J / Chen, Yan / Wang, Lizhen / Liu, Qian / Edge, Colin / Li, Yi / Dong, Kelly / Guan, Xiaoming / Tattersall, F David / Reith, Alastair D / Ren, Feng. ·Neurodegeneration DPU, Neurosciences Therapeutic Area Unit, GSK Pharmaceuticals R&D, 898 Halei Road, Zhangjiang Hi-Tech Park, Pudong, Shanghai 201203, PR China. · Neurodegeneration DPU, Neurosciences Therapeutic Area Unit, GSK Pharmaceuticals R&D, Medicines Research Centre, Gunnels Wood Road, Stevenage, Herts, UK. · Platform Technology Sciences, GSK Pharmaceuticals R&D, 898 Halei Road, Zhangjiang Hi-Tech Park, Pudong, Shanghai 201203, PR China. · Platform Technology Sciences, GSK Pharmaceuticals R&D, Medicines Research Centre, Gunnels Wood Road, Stevenage, Herts UK. · Neurodegeneration DPU, Neurosciences Therapeutic Area Unit, GSK Pharmaceuticals R&D, 898 Halei Road, Zhangjiang Hi-Tech Park, Pudong, Shanghai 201203, PR China. Electronic address: 2648666968@qq.com. ·Bioorg Med Chem Lett · Pubmed #30522952.

ABSTRACT: We describe the discovery and optimization of 5-substituted-N-pyridazinylbenzamide derivatives as potent and selective LRRK2 inhibitors. Extensive SAR studies led to the identification of compounds 18 and 23, which demonstrated good in vitro pharmacokinetic profile and excellent selectivity over 140 other kinases. Both compounds demonstrated high unbound fractions in both blood and brain. Compound 18 proved to be brain penetrant, and the high unbound fraction of compound 18 in brain enabled its in vivo efficacy in CNS, wherein a significant inhibition of LRRK2 Ser935 phosphorylation was observed in rat brain following intravenous infusion at 5 mg/kg/h.

5 Article Morphine reverses the effects of 1-methyl-4-phenylpyridinium in PC12 cells through activating PI3K/Akt. 2019

Fan, Yuan / Chen, Yan / Zhang, Se / Huang, Mengbing / Wang, Shengdong / Li, Ye / Bai, Jie. ·a Faculty of Environmental Science and Engineering , Kunming University of Science and Technology , Kunming , China. · b Medical Faculty , Kunming University of Science and Technology , Kunming , China. ·Int J Neurosci · Pubmed #29936883.

ABSTRACT: AIM OF THE STUDY: Parkinson's disease (PD) is a neurodegenerative disorder. It is caused by the degeneration of dopaminergic neurons and the dopamine (DA) deletion in the substantia nigra pars compacta (SNpc). Morphine elevates the level of dopamine in the mesolimbic dopamine system and plays a role in alleviating PD symptoms. However, the molecular mechanism is still unclear. The aim of the study is to investigate the mechanism on morphine alleviating PD symptoms. MATERIALS AND METHODS: The viability of PC12 cells was measured by using MTT assay. The expressions of tyrosine hydroxylase (TH), thioredoxin-1 (Trx-1), CyclinD1 and Cyclin-dependent kinase5 (Cdk5) were detected by Western Blot. RESULTS: In present study, we found that morphine increased the cell viability in PC12 cells. 1-methyl-4-phenylpyridi-nium (MPP+) reduced the cell viability and TH expression, which were reversed by morphine. MPP+ decreased the expressions of Trx-1, CyclinD1, Cdk5, which were restored by morphine. Moreover, the role of morphine in restoring the expressions of Trx-1, CyclinD1 and Cdk5 decreased by MPP+ was abolished by LY294002, phosphatidylinositol-3-kinase (PI3K)/Akt inhibitor. CONCLUSIONS: These results suggest that morphine reverses effects induced by MPP þ through activating PI3K/Akt pathway.

6 Article P75 Involved in the Ubiquitination of α-synuclein in Rotenone-based Parkinson's Disease Models. 2018

Chen, Yan / Hou, Yiwei / Yang, Jiaolong / Du, Ruofei / Chen, Chao / Chen, Fang / Wang, Hongcai / Ge, Ruli / Chen, Jinbo. ·Department of Gastroenterology, Affiliated Hospital of Binzhou Medical University, Binzhou City, Shandong Province, China. · Department of Neurology, Affiliated Hospital of Binzhou Medical University, Binzhou City, Shandong Province, China. · Department of Neurology, Renmin Hospital, Hubei University of Medicine, Shiyan 442000, Hubei Province, China. · University of New Mexico Comprehensive Cancer Center Biostatistics Shared Resource, New Mexico, USA. · Department of Neurology, Affiliated Hospital of Binzhou Medical University, Binzhou City, Shandong Province, China. Electronic address: whc2891@126.com. · Department of Neurology, Affiliated Hospital of Binzhou Medical University, Binzhou City, Shandong Province, China. Electronic address: gerli@163.com. · Department of Neurology, Affiliated Hospital of Binzhou Medical University, Binzhou City, Shandong Province, China. Electronic address: chenjinbo6720@126.com. ·Neuroscience · Pubmed #30081046.

ABSTRACT: For Parkinson's disease (PD), the regulatory mechanism of α-synuclein (α-syn) aggregation remains to be clarified. Ubiquitination modification is crucial for α-syn aggregation, with implications for Lewy body formation. Besides, ubiquitin ligase absentia homolog (siAH) is involved in the ubiquitination of α-syn. We investigated whether the p75 receptor can act as a potential regulator of α-syn accumulation through ubiquitination. Western blot, immunoprecipitation, gene transfection, and RNA interference technology were employed to detect the effect of p75 in in vivo and in vitro models. In a rotenone-based stereotactic (ST) infusion in vivo model of PD, p75 receptor and siAH expression was increased significantly compared with the control group. In cellular models of rotenone-mediated neurotoxicity, the interactions between p75 and siAH were revealed by immunoprecipitation; the colocalization of p75 with α-syn was observed in the cytoplasm; p75 promoted nuclear expression of NF-κB (p65), which might interact with the promoter of the siAH gene. Moreover, siRNA-mediated p75 depletion reduced the upregulation of α-syn and nuclear expression of p65 and protected against cell apoptosis induced by rotenone. Thus, aberrant expression of p75 may regulate the increased expression of α-syn, which is related to siAH-mediated ubiquitination and nuclear expression of p65.

7 Article Dysregulation of bcl-2 enhanced rotenone-induced α-synuclein aggregation associated with autophagic pathways. 2018

Chen, Yan / Zhang, Ningning / Ji, Dujuan / Hou, Yiwei / Chen, Chao / Fu, Yong / Ge, Ruli / Zheng, Qi / Chen, Jinbo / Wang, Hongcai. ·Departments of Gastroenterology. · Neurology, Affiliated Hospital of Binzhou Medical University, Binzhou City, China. ·Neuroreport · Pubmed #30059366.

ABSTRACT: α-Synuclein (α-syn) aggregation has far-reaching implications in the pathogenesis of Parkinson's disease, and the levels of α-syn protein determine its neurotoxic potential. However, the intrinsic pathway of α-syn accumulation and the mode of α-syn degradation remain contentious. Following a stereotactic infusion of rotenone into the substantia nigra and the ventral tegmental area, the chronic rat model of Parkinson's disease was established successfully. In response to the rotenone, increased intracellular α-syn levels and autophagic flux monitored by LC3 II turnover were induced in dopaminergic neurons (TH-positive) of rat substantia nigra and ventral tegmental area. In the cytoplasm, increased immune response of LC3 colocalized with α-syn on the basis of rotenone-mediated neurotoxicity. The immunoreactivity for p62, an adaptor of the autophagy, was upregulated in the cytoplasm and nucleus. The enhancement of autophagy by valproate acid decreased rotenone-induced α-syn aggregation, whereas the inhibition of autophagy by 3-methyladenine increased α-syn aggregation. In addition, the expression of bcl-2 was reduced in rotenone-induced neurotoxicity, accompanied by the enhancement of autophagy. Small interfering RNA-mediated knockdown of bcl-2 expression facilitated the expression of p62 protein and autophagy. Moreover, the inhibition of bcl-2 increased rotenone-based α-syn aggregation. In short, in rotenone-based models, dowregulation of bcl-2 negatively controlled rotenone-induced autophagy and α-syn aggregation.

8 Article Protective effect of roscovitine against rotenone-induced parkinsonism. 2018

Chen, Yan / Hou, Yiwei / Ge, Ruli / Han, Jianmei / Xu, Jing / Chen, Jinbo / Wang, Hongcai. ·Department of Gastroenterology, Affiliated Hospital of Binzhou Medical University, Shandong Province, China. · Department of Neurology, Affiliated Hospital of Binzhou Medical University, Shandong Province, China. · Department of Neurology, Yangxin County People's Hospital, Shandong Province, China. ·Restor Neurol Neurosci · Pubmed #30056439.

ABSTRACT: BACKGROUND: Protective effect of roscovitine and deregulation of the p-RB/E2F1 have not been well studied in PD models generated by repeated oral administration of rotenone. OBJECTIVE: These experiments evaluated the effects of repeated oral gavage of rotenone on the activation of p-RB/E2F1 and the effects of roscovitine on the regulation of dopaminergic neuronal injury and the behavior of PD in mice. METHODS: Using 2.5% carboxymethylcellulose and 1.25% chloroform as a vehicle solution, rotenone (30 mg/kg) was administered via oral gavage once daily for 30 days in C57 mice. Behavioral profiles (pole test and traction test) were assessed in these PD models, and oxidative stress levels were evaluated in the midbrain. The immunoreactivities of TH, α-synuclein (α-syn), p-RB, E2F1 and cleaved caspase-3 in the substantia nigra were examined with a laser confocal microscope. Pharmacological inhibition of cyclin-dependent kinase with roscovitine was achieved by intraperitoneal (IP) injection at a dose of 50 mg/kg daily. RESULTS: All rotenone-administered C57 mice showed the typical behavioral features of PD: stiffness, bradykinesia, or hypokinesia. Behavioral testing with the pole test and traction test indicated that the rotenone group, but not the vehicle group, was affected. Spectrophotometric analysis demonstrated that glutathione (GSH) and superoxide dismutase (SOD) activity was decreased, and the generation of malondialdehyde (MDA) was elevated in the midbrain of the rotenone-treated group. After oral administration of rotenone, a loss of nigral tyrosine hydroxylase (TH)-positive neurons was observed. The immune response of α-syn was enhanced in the cytoplasm of dopaminergic neurons from the rotenone-induced neurotoxicity. Rb phosphorylation at serine 780, which affected Rb binding to E2F, was induced after rotenone treatment. The activation of E2F1, which is involved in the regulation of the cell cycle, was also induced from chronic exposure to rotenone. Moreover, administration of the cell cycle inhibitor roscovitine protected against rotenone-induced nigral dopaminergic neuronal injury and inhibited cleaved caspase-3 activation. Roscovitine also markedly ameliorated the behavior of PD mice. CONCLUSIONS: Mouse models of Parkinson's disease were established by oral rotenone administration and reproduced some of the features of dopaminergic neuronal degeneration. Roscovitine protects against rotenone-induced parkinsonism.

9 Article Effects of Non-Pharmacological Treatments on Quality of Life in Parkinson's Disease: A Review. 2017

Ahn, Sangwoo / Chen, Yan / Bredow, Tim / Cheung, Corjena / Yu, Fang. ·University of Minnesota School of Nursing, Minneapolis, Minnesota. · Taihe Hospital, Hubei Province, China. · Department of Nursing, Bethel University, Arden Hills, MN 55112, USA. ·J Parkinsons Dis Alzheimers Dis · Pubmed #28932811.

ABSTRACT: Parkinson's disease is a neurodegenerative chronic condition with a declining trajectory and lack of a cure, making quality of life an important aspect of care. The purpose of this literature review was to analyze the state-of-the-science on the effects of non-pharmacological treatments on quality of life in person's with Parkinson's disease. Literature search was conducted using keywords in electronic databases up to September 1, 2016 and cross-searching the references of identified articles. Of the 259 articles generated, 26 met the eligibility criteria and were included in this review. The majority of studies (77%) were Level I evidence and 23% Level II evidence. The levels of study quality were: strong (50%), moderate (15%), and weak (35%). The interventions varied across studies with 15 studies evaluating a similar intervention. About 58% of the studies showed that the interventions improved quality of life. In conclusion, a variety of non-pharmacological interventions have been increasingly studied for their effects on quality of life in Parkinson's disease, showing initial promising results. However, most interventions were only examined by a limited number of studies and the minimal and optimal intervention doses needed for improving quality of life are yet unknown.

10 Article Subtypes evaluation of motor dysfunction in Parkinson's disease using neuromelanin-sensitive magnetic resonance imaging. 2017

Xiang, Yuanyuan / Gong, Tao / Wu, Junwei / Li, Jifeng / Chen, Yan / Wang, Yongxiang / Li, Shan / Cong, Lin / Lin, Youting / Han, Yuxiang / Yin, Ling / Wang, Guangbin / Du, Yifeng. ·Department of Neurology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong, PR China. · Shandong Medical Imaging Research Institute Affiliated to Shandong University, Jinan, Shandong, PR China. · Department of Orthopaedics, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong, PR China. · Shandong Medical Imaging Research Institute Affiliated to Shandong University, Jinan, Shandong, PR China. Electronic address: wgb7932596@hotmail.com. · Department of Neurology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong, PR China. Electronic address: 13173015523@163.com. ·Neurosci Lett · Pubmed #27993708.

ABSTRACT: Parkinson's disease (PD) is characterized by the loss of neuromelanin (NM)-containing neurons in the substantia nigra pars compacta (SNc), and it is divided into two motor subtypes: the postural instability gait difficulty (PIGD) and the tremor dominant (TD) subtypes. With NM-sensitive Magnetic Resonance Imaging (NM-MRI), investigators have been able to accurately detect signal attenuation in SNc of PD; however, the difference of NM loss between PIGD and TD subtypes is still unclear. Thus, the aim of this study was to evaluate the differences in NM-MRI between PD motor subtypes. PD patients were classified into PIGD (n=14) and TD groups (n=9); 20 age and sex matched controls were recruited. We compared the signal intensity contrast ratios in medial and lateral regions of the SNc using NM-MRI in PIGD, TD, and controls, respectively. Remarkable signal attenuation was observed in the lateral part of SNc in PD when compared with the controls, and we were able to detect more severe signal attenuation in the medial part of SNc in PIGD patients in comparison with that in the TD group. Also, the medial part of SNc, ipsilateral to the most clinically affected side, showed the highest power to discriminate the PD motor subtypes (AUC, 81%; sensitivity, 71.4%; specificity, 77.8%). Our results indicated a potential diagnostic value of NM-MRI to discriminate the PD motor subtypes, providing new evidence for the neuropathology-based differences between the two subtypes.

11 Article A clinical survey of pain in Parkinson's disease in Eastern China. 2016

Lin, Xing-Jian / Yu, Nian / Lin, Xiao-Guang / Zhang, Yan-Fang / Chen, Yan / Zhang, Kang / Wang, Xiao-Shan / Liu, Wei-Guo. ·Department of Neurology,Nanjing Brain Hospital,Nanjing Medical University,Nanjing,China. · Department of Neurology,Suqian People's Hospital,Jiangsu,China. ·Int Psychogeriatr · Pubmed #26443237.

ABSTRACT: BACKGROUND: This is a case-control study to investigate the prevalence, characteristics, and risk factors of pain in patients with Parkinson's disease (PD). METHODS: A total of 200 PD patients from eastern China were enrolled in our study. Accordingly, 200 healthy elderly adults were recruited as controls. The characteristics of pain were collected by using the Visual Analog Scale, Brief Pain Inventory (BPI), SF-36 Bodily Pain Scale, Unified Parkinson's Disease Rating Scale, Hoehn-Yahr Scale (H-Y), Hamilton Depression Scale, and Leeds Assessment of Neuropathic Symptoms and Signs. RESULTS: Of the 200 PD patients, pain was complained by 106 patients (53%). According to the SF-36 Bodily Pain Scale, pain morbidity in PD patients was significantly higher than in the control group. The average pain during last 24 h measured by the BPI was 2.67. About 76% of PD patients were found to have one pain type, 21.7% were having two pain types, and 1.9% had three pain types. Further, 69.8% of these patients were presented with musculoskeletal pain, 4.7% with dystonic pain, 22.6% with radicular-neuropathic pain, 20.8% with central neuropathic pain, and 9.4% with akathisia pain. The onset age and depression were the most significant predictors of pain in PD patients (p < 0.05). However, there was no significant association between pain and gender, age, disease duration, or severity of the disease. Only 5.7% of PD patients with pain received treatment in this study. CONCLUSIONS: Pain is frequent and disabling, independent of demographic and clinical variables, and is significantly more common in PD patients.

12 Article Involvement of mortalin/GRP75/mthsp70 in the mitochondrial impairments induced by A53T mutant α-synuclein. 2015

Liu, Feng-Tao / Chen, Yan / Yang, Yu-Jie / Yang, Ling / Yu, Mei / Zhao, Jian / Wu, Jian-Jun / Huang, Fang / Liu, Wen / Ding, Zheng-Tong / Wang, Jian. ·Department of Neurology, Huashan Hospital Affiliated to Fudan University, 12 Wulumuqi Middle Road, Shanghai 200040, China; Department & Institute of Neurology, Shanghai Medical College, Fudan University, Shanghai 200040, China. Electronic address: liuft110@aliyun.com. · Department of Neurology, Huashan Hospital Affiliated to Fudan University, 12 Wulumuqi Middle Road, Shanghai 200040, China; Department & Institute of Neurology, Shanghai Medical College, Fudan University, Shanghai 200040, China. Electronic address: chhyann@gmail.com. · Department of Cellular and Genetic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China. Electronic address: yujieyang1015@me.com. · Department of Cellular and Genetic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China. Electronic address: yangling@fudan.edu.cn. · State Key Laboratory of Medical Neurobiology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China. Electronic address: yumei@fudan.edu.cn. · Department of Neurology, Huashan Hospital Affiliated to Fudan University, 12 Wulumuqi Middle Road, Shanghai 200040, China; Department & Institute of Neurology, Shanghai Medical College, Fudan University, Shanghai 200040, China. Electronic address: zhaojian20052006@163.com. · Department of Neurology, Huashan Hospital Affiliated to Fudan University, 12 Wulumuqi Middle Road, Shanghai 200040, China; Department & Institute of Neurology, Shanghai Medical College, Fudan University, Shanghai 200040, China. Electronic address: jungliw@gmail.com. · State Key Laboratory of Medical Neurobiology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China; Institutes of Brain Science, Fudan University, Shanghai 200032, China. Electronic address: huangf@shmu.edu.cn. · Department of Cellular and Genetic Medicine, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China. Electronic address: liuwen@shmu.edu.cn. · Department of Neurology, Huashan Hospital Affiliated to Fudan University, 12 Wulumuqi Middle Road, Shanghai 200040, China; Department & Institute of Neurology, Shanghai Medical College, Fudan University, Shanghai 200040, China. Electronic address: zhtding@hotmail.com. · Department of Neurology, Huashan Hospital Affiliated to Fudan University, 12 Wulumuqi Middle Road, Shanghai 200040, China; Department & Institute of Neurology, Shanghai Medical College, Fudan University, Shanghai 200040, China. Electronic address: wangjian336@hotmail.com. ·Brain Res · Pubmed #25665531.

ABSTRACT: Mutations and excessive accumulation of α-synuclein (α-syn) can lead to the degeneration of dopaminergic neurons, indicating a pivotal role of α-syn in the pathogenesis of Parkinson's disease (PD). Although how α-syn contributes to PD is still elusive, mitochondrial impairments have been reported to be implicated in. Mortalin, a molecular chaperone mainly located in mitochondria, has been linked to the pathogenesis of PD in recent studies. Moreover, some proteomics studies indicate that mortalin is associated with PD-related proteins, including α-syn. Therefore it is of interest to understand the function of mortalin in the mitochondrial disruption induced by A53T α-syn overexpression. The present study modulated the expression of mortalin and detected the effect of mortalin on the mitochondrial impairments induced by A53T α-syn in SH-SY5Y cells. Our data revealed that A53T α-syn could disrupt mitochondrial dynamics and increase the neuronal susceptibility to neurotoxin rotenone. The expression of mortalin decreased significantly in dopaminergic cells overexpressing A53T α-syn; furthermore, the down-regulation of mortalin could attenuate the disrupted mitochondrial dynamics by reducing α-syn translocation to mitochondria, suggesting that a compensatory mechanism of mortalin might be implicated in the pathogenesis of PD.