Alpha-Synuclein Transmission and Mitochondrial Toxicity in Primary Human Foetal Enteric Neurons In Vitro View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2013-09-12

AUTHORS

Nady Braidy, Wei-Ping Gai, Ying Hua Xu, Perminder Sachdev, Gilles J. Guillemin, Xing-Mai Jiang, J. William O. Ballard, Martin P. Horan, Zhi Ming Fang, Beng H. Chong, Daniel Kam Yin Chan

ABSTRACT

Parkinson’s disease (PD) is a multicentred neurodegenerative disorder characterised by the accumulation and aggregation of alpha-synuclein (α-syn) in several parts of the central nervous system. However, it is well established that PD can generate symptoms of constipation and other gastrointestinal problems and α-syn containing lesions have been identified in intestinal nerve cells. In this study, we show that α-syn can be taken up and accumulate in primary human foetal enteric neurons from the gastrointestinal tract and can be transferred between foetal enteric neurons. Impaired proteosomal/lysosomal degradation can promote the uptake and accumulation of α-syn in enteric neurons. Enteric neurons exposed to α-syn can also lead to impaired mitochondrial complex I activity, reduced mitochondrial function, and NAD+ depletion culminating in cell death via energy restriction. These findings demonstrate neuron-to-neuron transmission of α-syn in enteric neurons, providing renewed evidence for Braak’s hypothesis and the aetiology of PD. More... »

PAGES

170-182

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s12640-013-9420-5

DOI

http://dx.doi.org/10.1007/s12640-013-9420-5

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1053321709

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/24026637


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