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

Research output: Contribution to journal › Article › peer-review

69 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

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

Keywords

Alpha-synuclein
Astrocytes
Fibroblasts
Mitochondria
Neurons

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1186/2047-9158-2-20

Cite this

@article{96578ec9e6724491b347ffb824e6ff8c,

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

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.",

keywords = "Alpha-synuclein, Astrocytes, Fibroblasts, Mitochondria, Neurons",

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

year = "2013",

month = oct,

day = "4",

doi = "10.1186/2047-9158-2-20",

language = "English",

volume = "2",

journal = "Translational Neurodegeneration",

issn = "2047-9158",

publisher = "BioMed Central",

number = "1",

}

TY - JOUR

T1 - Uptake and mitochondrial dysfunction of alpha-synuclein in human astrocytes, cortical neurons and fibroblasts

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

PY - 2013/10/4

Y1 - 2013/10/4

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.

KW - Alpha-synuclein

KW - Astrocytes

KW - Fibroblasts

KW - Mitochondria

KW - Neurons

UR - http://www.scopus.com/inward/record.url?scp=84886254944&partnerID=8YFLogxK

U2 - 10.1186/2047-9158-2-20

DO - 10.1186/2047-9158-2-20

M3 - Article

SN - 2047-9158

VL - 2

JO - Translational Neurodegeneration

JF - Translational Neurodegeneration

IS - 1

M1 - 20

ER -

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

Abstract

Bibliographical note

Keywords

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this