title: Comparison between α-synuclein wild-type and A53T mutation in a progressive Parkinson's disease model.
abstract: OBJECTIVE
  Vector based over-expression of α-synuclein is a newly developed method to establish animal Parkinson's disease (PD) model. In this paper, we inject the rat brain with recombinant adeno-associated virus (rAAV) to express α-synuclein wild-type and A53T mutation, and compared the degeneration of dopaminergic neurons between them.
  
  
  RESULTS
  The rAAV vectors were injected into the substantia nigra pars compacta (SNpc) of rat brain. In different time point, immunohistochemistry was used to detect the expression of α-synuclein. The expression level was lower in the 3rd and 6th week and increased from the 9th week. α-synuclein spread around the neurons in SNpc in the 12th week. The loss of dopaminergic neurons was increasing along the expression of α-synuclein, and damage extent was more serious in the A53T group than the WT group. In the A53T group, there were more insoluble inclusions can be detected, and the phosphorylation of α-synuclein was also higher.
  
  
  CONCLUSIONS
  The result of comparison between the two types of α-synuclein showed that A53T mutated α-synuclein was more effective to establish PD model, and the model based A53T mutated α-synuclein was a suitable model to early-onset PD.
authors.affiliation: School of Life Science, Beijing Institute of Technology, 5 South Zhongguancun Street, Haidian District, Beijing 100081, People's Republic of China.
authors.forename: Jianqing
authors.initials: J
authors.lastname: Lu
authors.affiliation: School of Life Science, Beijing Institute of Technology, 5 South Zhongguancun Street, Haidian District, Beijing 100081, People's Republic of China.
authors.forename: Feiyi
authors.initials: F
authors.lastname: Sun
authors.affiliation: School of Life Science, Beijing Institute of Technology, 5 South Zhongguancun Street, Haidian District, Beijing 100081, People's Republic of China.
authors.forename: Hong
authors.initials: H
authors.lastname: Ma
authors.affiliation: School of Life Science, Beijing Institute of Technology, 5 South Zhongguancun Street, Haidian District, Beijing 100081, People's Republic of China.
authors.forename: Hong
authors.initials: H
authors.lastname: Qing
authors.affiliation: School of Life Science, Beijing Institute of Technology, 5 South Zhongguancun Street, Haidian District, Beijing 100081, People's Republic of China. Electronic address: deng@bit.edu.cn.
authors.forename: Yulin
authors.initials: Y
authors.lastname: Deng
mesh_terms: D000367:Age Factors; D019943:Amino Acid Substitution; D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D001921:Brain / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D059290:Dopaminergic Neurons / Q000378:metabolism / Q000473:pathology; D007150:Immunohistochemistry; D008297:Male; D050505:Mutant Proteins / Q000235:genetics* / Q000378:metabolism*; D020125:Mutation, Missense; D020734:Parkinsonian Disorders / Q000209:etiology / Q000235:genetics* / Q000378:metabolism*; D010766:Phosphorylation; D066263:Protein Aggregation, Pathological / Q000235:genetics / Q000378:metabolism; D051381:Rats; D055647:Rats, Transgenic; D017208:Rats, Wistar; D011994:Recombinant Proteins / Q000235:genetics / Q000378:metabolism; D014102:Torsion Abnormality / Q000209:etiology / Q000503:physiopathology; D051844:alpha-Synuclein / Q000235:genetics* / Q000378:metabolism*
chemical_list: D050505:Mutant Proteins; D011994:Recombinant Proteins; D051844:alpha-Synuclein; D001058:Apomorphine
keywords: Animal model; Parkinson's disease; Recombinant adeno-associated virus; α-synuclein