Uptake and mitochondrial dysfunction of alpha-synuclein in human astrocytes, cortical neurons and fibroblasts

Translational Neurodegeneration

Daniel Kam Yin Chan⁷  Beng H Chong³  Zhi Ming Fang³  Martin P Horan²  J William O Ballard²  Xing-Mai Jiang³  Gilles J Guillemin⁴  Perminder Sachdev⁵  Ying Hua Xu⁶  Wei-Ping Gai⁷  Nady Braidy¹ 

[1] Aged Care and Rehabilitation, Bankstown-Lidcombe Hospital, Sydney, Australia;School of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, Australia;St George Clinical School, University of New South Wales and St George Hospital, Sydney, Australia;St Vincent’s Centre for Applied Medical Research, Sydney, Australia;Neuropsychiatric Institute, Prince of Wales Hospital, Sydney, Australia;Faculty of Medicine, University of New South Wales, Sydney, Australia;Department of Human Physiology and Centre for Neuroscience, Flinders University School of Medicine, Adelaide, Australia

关键词: Mitochondria;    Fibroblasts;    Astrocytes;    Neurons;    Alpha-synuclein;   

Others  :  838556
DOI  :  10.1186/2047-9158-2-20

 received in 2013-06-03, accepted in 2013-10-01,  发布年份 2013

【 摘 要 】

The accumulation and aggregation of alpha-synuclein (α-syn) in several tissue including the brain is a major pathological hallmark in Parkinson’s disease (PD). In this study, we show that α-syn can be taken up by primary human cortical neurons, astrocytes and skin-derived fibroblasts in vitro. Our findings that brain and peripheral cells exposed to α-syn can lead to impaired mitochondrial function, leading to cellular degeneration and cell death, provides additional evidence for the involvement of mitochondrial dysfunction as a mechanism of toxicity of α-syn in human cells.

【 授权许可】

   
2013 Braidy et al.; licensee BioMed Central Ltd.

【 图 表 】

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