期刊论文详细信息
NEUROSCIENCE LETTERS 卷:711
Trichloroethylene and its metabolite TaClo lead to degeneration of substantia nigra dopaminergic neurones: Effects in wild type and human A30P mutant α-synuclein mice
Article
Keane, P. C.1,2  Hanson, P. S.1  Patterson, L.2,3  Blain, P. G.1  Hepplewhite, P.2  Khundakar, A. A.2  Judge, S. J.1,2  Kahle, P. J.4  LeBeau, F. E. N.2  Morris, C. M.1,2,3 
[1] Newcastle Univ, Med Toxicol Ctr, Wolfson Bldg,Claremont Pl, Newcastle Upon Tyne NE2 4AA, Tyne & Wear, England
[2] Newcastle Univ, Inst Neurosci, Cookson Bldg,Framlington Pl, Newcastle Upon Tyne NE2 4HH, Tyne & Wear, England
[3] Newcastle Univ, Alzheimers Soc Doctoral Training Ctr, Edwardson Bldg, Newcastle Upon Tyne NE4 5PL, Tyne & Wear, England
[4] Univ Tubingen, German Ctr Neurodegenerat Dis DZNE Tubingen, Hertie Inst Clin Brain Res, Lab Funct Neurogenet, D-72076 Tubingen, Germany
关键词: Trichloroethylene;    TaClo;    Parkinson's disease;    alpha-Synuclein;    Neurodegeneration;   
DOI  :  10.1016/j.neulet.2019.134437
来源: Elsevier
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【 摘 要 】

Parkinson's disease (PD) is characterised pathologically by degeneration of the dopaminergic (DA) neurones of the substantia nigra pars compacta (SNpc) and the presence of alpha-synuclein containing Lewy body inclusions. Trichloroethylene (TCE) has been suggested as a potential environmental chemical that may contribute to the development of PD, via conversion to the neurotoxin, 1-Trichloromethyl-1,2,3,4-tetrahydro-beta-carboline (TaClo). We investigated the effect of an 8 week exposure to TCE or TaClo on wild type and, as an experimental model of PD, A30P mutant alpha-synuclein overexpressing mice using a combination of behaviour and pathology. TCE or TaClo exposure caused significant DA neuronal loss within the SNpc in both wild type and transgenic mice. Cell numbers were lower in A30P animals than wild type, however, no additive effect of TCE or TaClo exposure and A30P overexpression was found. TCE or TaClo did not appear to lead to acceleration of motor or cognitive deficits in either wild type or A30P mutant mice, potentially because of the modest reductions of DA neuronal number in the SNpc. Our results do however suggest that TCE exposure could be a possible factor in development of PD like changes following exposure.

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