| Literature DB >> 26490328 |
Jin H Nam1, Eun S Park1, So-Yoon Won2, Yu A Lee1, Kyoung I Kim1, Jae Y Jeong1, Jeong Y Baek1, Eun J Cho1, Minyoung Jin1, Young C Chung1, Byoung D Lee1, Sung Hyun Kim1, Eung-Gook Kim2, Kyunghee Byun3, Bonghee Lee3, Dong Ho Woo4, C Justin Lee4, Sang R Kim5, Eugene Bok6, Yoon-Seong Kim7, Tae-Beom Ahn8, Hyuk Wan Ko1, Saurav Brahmachari9, Olga Pletinkova10, Juan C Troconso11, Valina L Dawson12, Ted M Dawson13, Byung K Jin14.
Abstract
Currently there is no neuroprotective or neurorestorative therapy for Parkinson's disease. Here we report that transient receptor potential vanilloid 1 (TRPV1) on astrocytes mediates endogenous production of ciliary neurotrophic factor (CNTF), which prevents the active degeneration of dopamine neurons and leads to behavioural recovery through CNTF receptor alpha (CNTFRα) on nigral dopamine neurons in both the MPP(+)-lesioned or adeno-associated virus α-synuclein rat models of Parkinson's disease. Western blot and immunohistochemical analysis of human post-mortem substantia nigra from Parkinson's disease suggests that this endogenous neuroprotective system (TRPV1 and CNTF on astrocytes, and CNTFRα on dopamine neurons) might have relevance to human Parkinson's disease. Our results suggest that activation of astrocytic TRPV1 activates endogenous neuroprotective machinery in vivo and that it is a novel therapeutic target for the treatment of Parkinson's disease.Entities:
Keywords: Parkinson’s disease; TRPV1; astrocyte; ciliary neurotrophic factor (CNTF); dopamine neurons
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Year: 2015 PMID： 26490328 PMCID： PMC4840550 DOI： 10.1093/brain/awv297
Source DB: PubMed Journal: Brain ISSN： 0006-8950 Impact factor: 13.501