Journal of Gannan Medical University

References

[1] de Rijk MC,Launer LJ,Berger K,et al.Prevalence of Parkinson's disease in Europe:a collaborative study of population-based cohorts[J].Neurology,2000,54(11):S21-3.

[2] Zassoj,Ahmedm,Cutarellia,et al.Inducible alpha-synuclein expression affects human neural stem cells′behavior[J].StemCellsDev,2018,27(14):985-994.

[3] Shamoto-Nagai M,Hisaka S,Naoi M,et al.Modification of α-synuclein by lipid peroxidation products derived from polyunsaturated fatty acids promotes toxic oligomerization:its relevance to Parkinson disease[J].J Clin Biochem Nutr,2018,62(3):207-212.

[4] Emmanouilid,Vekrellisk.Exocytosis and spreading of normal and aberrant α-synuclein[J].Brain Pathology,2016,26(3):398-403.

[5] Svensson E,Horváth-Puhó E,Thomsen RW,et al.Vagotomy and subsequent risk of Parkinson's disease[J].Ann Neurol,2015,78(4):522-529.

[6] Kaushik S,Cuervo A M.Proteostasis and aging[J].Nat Med,2015,21:1406-1415.

[7] Ganguly G,Chakrabarti S,Chatterjec U,et al.Proteinopathy,oxidative stress and mitochondrial dysfunction:cross talk in Alzheimer's disease and Parkinson's disease[J].Drug Des Devel Ther,2017,11:797-810.

[8] Tanik S A,Schultheiss C E,Volpicelli-Daley,et al.Lewy body-like alphasynuclein aggregates resist degradation and impair macroautophagy[J].Biol Chem,2013,288:15194-15210.

[9] Nalls M.A.Large-scale meta-analysis of genomewide association data identifies six new risk loci for Parkinson's disease[J].Nat Genet,2014,46:989-993.

[10] Belluccia,Navarrial,Zaltierim,et al.Alpha-synuclein synaptic pathology and its implications in thedevelopment of novel therapeutic approaches to cure Parkinson's disease[J].Brain Res,2012,1432:95-113.

[11] Volpicelli-Daley L.A.G2019S-LRRK2 expression augments alpha-synuclein sequestration into inclusions in neurons[J].Neurosci,2016,36:7415-7427.

[12] Fernandes H.J.ER stress and autophagic perturbations lead to elevated extracellular alphasynuclein in GBA-N370S Parkinson's iPSC-derived dopamine neurons[J].Stem Cell Reports,2016,6:342-356.

[13] Sardi S P.Augmenting CNS glucocerebrosidase activity as a therapeutic strategy for parkinsonism and other Gaucher-related synucleinopathies[J].Proc Natl Acad Sci USA,2013,110(9):3537-3542.

[14] Tang F L.VPS35 in dopamine neurons is required for endosome-to-golgi retrieval of Lamp2a,a receptor of chaperone-mediated autophagy that is critical for alpha-synuclein degradation and prevention of pathogenesis of Parkinson's disease[J].Neurosci,2015,3(5):10613-10628.

[15] Dhungel N.Parkinson's disease genes VPS35 and EIF4G1 interact genetically and converge on alpha-synuclein[J].Neuron,2015,85:76-87.

[16] Bose A,Beal M F.Mitochondrial dysfunction in Parki-nson's disease[J].Neurochem,2016,139 (1):216-231.

[17] Gautier CA,Corti O,Brice A.Mitochondrial dysfunctions in Parkinson's disease[J].Rev Neurol (Paris),2014,170:339-343.

[18] 杨智明,李煦照,卢芳,等.帕金森病的线粒体发病机制研究进展[J].中国老年学杂志,2014,34:6233.

[19] Diasv,Junne,Mouradianmm.The role of oxidative stress in Parkinson's disease[J].J Parkinsons Dis,2013,3(4):461-491.

[20] Eschbach J.Mutual exacerbation of peroxisome proliferator-activated receptor gamma coactivator1alpha deregulation and alpha-synuclein oligomerization[J].Ann Neurol,2015,77:15-32.

[21] Zheng B.PGC-1alpha,a potential therapeutic target for early intervention in Parkinson's disease[J].Sci Transl Med,2010,2:52ra73.

[22] Sen A,Kalvakuris,Bodmerr,et al.Clueless,a protein required for mitochondrial function,interacts with the PINK1-Parkin complex in drosophila[J].Dis Model Mech,2015,8(6):577-589.

[23] Ylonen S,Ylikotila P,Siitonen A,et al.Variations of mitochondrial DNA polymerase gamma in patients with Parkinson's disease[J].Neurol,2013,260:3144-3149.

[24] Bose A,Beal M F.Mitochondrial dysfunction in Parkinson's disease[J].Neurochem,2016,139(1):216-231.

[25] Schapira AH,Jenner P.Etiology and pathogenesis of Parkinson's disease[J].Mov Disord,2011,26:1049-1055.

[26] Ren X,Zou L,Zhang X,et al.Redox signaling mediated by thioredoxin and glutathione systems in the central nervous system[J].Antioxid Redox Signal,2017,27(1):989-1010.

[27] Michell-Robinson MA,Touil H,Healy LM,et al.Roles of microglia in brain development,tissue maintenance and repair[J].Brain:a journal of neurology,2015,138:1138-1159.

[28] Hu X,Leak RK,Shi Y,et al.Microglial and macrophage polarization-new prospects for brain repair[J].Nature reviews Neurology,2015,11(1):56-64.

[29] Chao Y,Wong SC,Tan EK.Evidence of inflammatory system involvement in Parkinson's disease[J].Biomed Res Int,2014,2014:308654.

[30] 许加军,杨洪安,王国栋,等.胶质细胞源性神经营养因子对帕金森病大鼠多巴胺能神经元的修复作用[J].山东医药,2014,54 (34):21-23.

[31] Hemptinne C,Swann NC,Ostrem JL,et al.Therapeutic deep brain stimulation reduces cortical phase-amplitude coupling in Parkinson' s disease[J].Nat Neurosci,2015,18(5) :779-786.

[32] Olanow CW,Wakeman DR,Kordower JH.Peripheral alpha-synuclein and Parkinson's disease[J].Mov Disord,2014,29(8):963-966.

[33] Ransohoff R M.How neuroinflammation contributes to neurodegeneration[J].Science,2016,353:777-783.

[34] Gao H M.Neuroinflammation and oxidation/ nitration of alpha-synuclein linked to dopaminergic neurodegeneration[J].Neurosci,2008,28:7687-7698.

[35] Cebrian C.MHC-I expression renders catecholaminergic neurons susceptible to T-cellmediated degeneration[J].Nat Commun,2014,5:3633.

[36] George S,Brundin P.Immunotherapy in Parkinson's disease:micromanaging alpha-synuclein aggregation[J].Parkinsons Dis,2015,5:413-424.