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

Nady Braidy; Wei-Ping Gai; Ying Hua Xu; Perminder Sachdev; Gilles Guillemin; Xing-Mai Jiang; J Ballard; Martin Horan; Zhi Ming Fang; Beng Chong; Daniel Chan

doi:10.1186/2047-9158-2-20

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

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

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80 Citations (Scopus)

Abstract

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.

Original language	English
Article number	20
Number of pages	9
Journal	Translational Neurodegeneration
Volume	2
Issue number	1
DOIs	https://doi.org/10.1186/2047-9158-2-20
Publication status	Published - 4 Oct 2013

Bibliographical note

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Copyright 2013 Elsevier B.V., All rights reserved.

Keywords

Alpha-synuclein
Astrocytes
Fibroblasts
Mitochondria
Neurons

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abstract = "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.",

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AU - Braidy, Nady

AU - Gai, Wei-Ping

AU - Xu, Ying Hua

AU - Sachdev, Perminder

AU - Guillemin, Gilles

AU - Jiang, Xing-Mai

AU - Ballard, J

AU - Horan, Martin

AU - Fang, Zhi Ming

AU - Chong, Beng

AU - Chan, Daniel

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N2 - 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.

AB - 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.

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KW - Astrocytes

KW - Fibroblasts

KW - Mitochondria

KW - Neurons

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

Abstract

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Keywords

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