Journal of Neural Transmission-supplement最新文献_第8页

Therapeutic drug monitoring of antidepressants--clinical aspects. 抗抑郁药的治疗药物监测——临床方面。

Journal of Neural Transmission-supplement Pub Date : 2007-01-01 DOI: 10.1007/978-3-211-73574-9_32

G. Laux, P. Baumann, C. Hiemke

引用次数: 15

CYP 2E1 mutant mice are resistant to DDC-induced enhancement of MPTP toxicity. CYP 2E1突变小鼠对ddc诱导的MPTP毒性增强具有抗性。

Journal of Neural Transmission-supplement Pub Date : 2007-01-01 DOI: 10.1007/978-3-211-73574-9_20

C Viaggi, F Vaglini, C Pardini, P Sgadò, A Caramelli, G U Corsini

引用次数: 5

Low dose methylphenidate improves freezing in advanced Parkinson's disease during off-state. 低剂量哌醋甲酯改善晚期帕金森病非状态期间的冷冻。

Journal of Neural Transmission-supplement Pub Date : 2007-01-01 DOI: 10.1007/978-3-211-73574-9_17

L Pollak, Y Dobronevsky, T Prohorov, S Bahunker, J M Rabey

引用次数: 49

Genetic analysis of dopaminergic system development in zebrafish. 斑马鱼多巴胺能系统发育的遗传分析。

Journal of Neural Transmission-supplement Pub Date : 2006-01-01 DOI: 10.1007/978-3-211-45295-0_11

S Ryu, J Holzschuh, J Mahler, W Driever

引用次数: 36

Relationship between axonal collateralization and neuronal degeneration in basal ganglia. 基底神经节轴突侧支与神经元变性的关系。

Journal of Neural Transmission-supplement Pub Date : 2006-01-01 DOI: 10.1007/978-3-211-45295-0_14

M Parent, A Parent

引用次数: 44

Parkin and defective ubiquitination in Parkinson's disease. 帕金森病与泛素化缺陷。

Journal of Neural Transmission-supplement Pub Date : 2006-01-01 DOI: 10.1007/978-3-211-45295-0_32

T M Dawson

{"title":"Parkin and defective ubiquitination in Parkinson's disease.","authors":"T M Dawson","doi":"10.1007/978-3-211-45295-0_32","DOIUrl":"https://doi.org/10.1007/978-3-211-45295-0_32","url":null,"abstract":"Parkinson's Disease (PD) is a common neurodegenerative disorder that is characterized by the progressive loss of dopamine (DA) neurons. Accompanying the loss the of DA neurons is the accumulation of Lewy bodies and neurites, intracytoplasmic proteinaceous inclusions that contain alpha-synuclein, synphilin-1, components of the ubiquitin proteasomal pathway and parkin. Recent advances indicate that PD is due in some individuals to genetic mutations in alpha-synuclein, DJ-1, PINK-1, LRRK2, and parkin. Understanding the molecular mechanisms by which mutations in familial-linked genes cause PD holds great promise for unraveling the mechanisms by which DA neurons degenerate in PD. Parkin is E3-ubiquitin-protein ligase that ubiquitinates itself and promotes its own degradation. Familial associated mutations of parkin have impaired ubiquitin ligase function suggesting that this may be the cause of familial autosomal recessive PD. Parkin might be required for formation of Lewy bodies as Lewy bodies are absent in patients with parkin mutations. Parkin interacts with and ubiquitinates the alpha-synuclein interacting protein, synphilin-1. Formation of Lewy-body-like ubiquitin-positive cytosolic inclusions occurs upon coexpression of alpha-synuclein, synphilin-1 and parkin. Nitric oxide inhibits Parkin's E-3 ligase activity and its protective function by nitric oxide through S-nitrosylation both in vitro and in vivo. Nitrosative and oxidative stress link parkin function with the more common sporadic form of Parkinson's disease and the related alpha-synucleinopathy, DLBD. Development of new therapies for PD and other disorders associated with nitrosative and oxidative stress may follow the elucidation of the pathways by which NO S-nitrosylates and inhibits parkin. Moreover, parkin and alpha-synuclein are linked in common pathogenic mechanism through their interaction with synphilin-1 and parkin may be important for the formation of Lewy bodies.","PeriodicalId":16395,"journal":{"name":"Journal of Neural Transmission-supplement","volume":" 70","pages":"209-13"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/978-3-211-45295-0_32","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26288828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 76

Alpha-synuclein overexpression model. α -突触核蛋白过表达模型。

Journal of Neural Transmission-supplement Pub Date : 2006-01-01

H Mochizuki, M Yamada, Y Mizuno

{"title":"Alpha-synuclein overexpression model.","authors":"H Mochizuki, M Yamada, Y Mizuno","doi":"","DOIUrl":"","url":null,"abstract":"Objectives: To elucidate the role of alpha-synuclein in the pathogenesis of Parkinson's disease (PD), both human alpha-synuclein transgenic mice and targeted overexpression of human alpha-synuclein in rat substantia nigra (SN) by viral vector-based methods have been studied, however little is known about the pathogenetic changes of dopaminergic neuron loss. Therefore, it is necessary to address whether the pathogenetic changes in the brains of patients with PD are recapitulated in these models.Methods and results: We used the recombinant adeno-associated viral (rAAV) vector system for human alpha-synuclein gene transfer to rat SN and observed approximately 50% loss of dopaminergic neurons in SN at 13 weeks after infection. In the slower progression of neurodegeneration, we identified several important features in common with the pathogenesis of PD, such as phosphorylation of alpha-synuclein at Ser129 and activation of caspase-9. Both findings were also evident in cortical tissues overexpressing alpha-synuclein via rAAV.Conclusions: Our results indicate that overexpression of alpha-synuclein via rAAV apparently recapitulates several important features of brains with PD and dementia with Lewy bodies (DLB), and thus alpha-synucleinopathy described here is likely to be an ideal model for the study of the pathogenesis of PD and DLB. This model is also useful for the gene therapy research.","PeriodicalId":16395,"journal":{"name":"Journal of Neural Transmission-supplement","volume":" 70","pages":"281-4"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26344642","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Triggering endogenous neuroprotective mechanisms in Parkinson's disease: studies with a cellular model. 帕金森病触发内源性神经保护机制:细胞模型研究

Journal of Neural Transmission-supplement Pub Date : 2006-01-01 DOI: 10.1007/978-3-211-45295-0_66

M J Zigmond

引用次数: 16

Genetics of dystonia. 肌张力障碍的遗传学。

Journal of Neural Transmission-supplement Pub Date : 2006-01-01 DOI: 10.1007/978-3-211-45295-0_73

S Bressman

引用次数: 10

Critical appraisal of brain pathology staging related to presymptomatic and symptomatic cases of sporadic Parkinson's disease. 散发性帕金森病症状前和症状性病例脑病理分期的关键评价

Journal of Neural Transmission-supplement Pub Date : 2006-01-01 DOI: 10.1007/978-3-211-45295-0_16

G M Halliday, K Del Tredici, H Braak

引用次数: 104