Xing-Mai Jiang
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Xing-Mai Jiang has a total of 10 co-authors. Here are the top co-authors by number of shared publications:
- Beng H. Chong
University of New South Wales
1 shared publication - Daniel Leonard Chan
Department of Surgery, St George Hospital, Sydney, New South Wales, Australia
1 shared publication - Gilles Jackie Guillemin
Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Macquarie University, Sydney, Australia
1 shared publication - John William Oman Ballard
School of Biosciences, University of Melbourne , Royal Parade, Parkville, Victoria 3052
1 shared publication - Martin P. Horan
Institute of Medical Genetics, School of Medicine, Cardiff University, Cardiff, CF14 4XN, UK,
1 shared publication - Nady Braidy
Centre for Healthy Brain Ageing (CHeBA), School of Psychiatry, Faculty of Medicine, University of New South Wales, Sydney, Australia
1 shared publication
Latest Publications
- Open Access
- 4 October 2013
- Published by Springer Nature in Translational Neurodegeneration
- Vol. 2 (1) , 20
Uptake and mitochondrial dysfunction of alpha-synuclein in human astrocytes, cortical neurons and fibroblasts
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 fibroblastsin 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.
- 4 October 2013
- Published by Springer Nature in Translational Neurodegeneration
- Vol. 2 (1) , 20
Open AccessUptake and mitochondrial dysfunction of alpha-synuclein in human astrocytes, cortical neurons and fibroblasts
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 fibroblastsin 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.