Intranasal LPS-mediated Parkinson's model challenges the pathogenesis of nasal cavity and environmental toxins.

Accumulating evidence implicates the relationship between neuroinflammation and pathogenesis in idiopathic Parkinson's disease (iPD). The nose has recently been considered a gate way to the brain which facilitates entry of environmental neurotoxin into the brain. Our study aims to build a PD mo...

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Main Authors: Qing He, Wenbo Yu, Jianjun Wu, Chan Chen, Zhiyin Lou, Qiong Zhang, Jian Zhao, Jian Wang, Baoguo Xiao
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2013-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC3826714?pdf=render
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spelling doaj-994de0b9f2e64c4f975f12c142c3fe772020-11-25T02:11:57ZengPublic Library of Science (PLoS)PLoS ONE1932-62032013-01-01811e7841810.1371/journal.pone.0078418Intranasal LPS-mediated Parkinson's model challenges the pathogenesis of nasal cavity and environmental toxins.Qing HeWenbo YuJianjun WuChan ChenZhiyin LouQiong ZhangJian ZhaoJian WangBaoguo XiaoAccumulating evidence implicates the relationship between neuroinflammation and pathogenesis in idiopathic Parkinson's disease (iPD). The nose has recently been considered a gate way to the brain which facilitates entry of environmental neurotoxin into the brain. Our study aims to build a PD model by a natural exposure route. In this report, we establish a new endotoxin-based PD model in mice by unilateral intranasal (i.n.) instillation of the lipopolysaccharides (LPS) every other day for 5 months. These mice display a progressive hypokinesia, selective loss of dopaminergic neurons, and reduction in striatal dopamine (DA) content, as well as α-synuclein aggregation in the SN, without systemic inflammatory and immune responses. This new PD model provides a tool for studying the inflammation-mediated chronic pathogenesis and searching for therapeutic intervention in glia-neuron pathway that will slow or halt neurodegeneration in PD.http://europepmc.org/articles/PMC3826714?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Qing He
Wenbo Yu
Jianjun Wu
Chan Chen
Zhiyin Lou
Qiong Zhang
Jian Zhao
Jian Wang
Baoguo Xiao
spellingShingle Qing He
Wenbo Yu
Jianjun Wu
Chan Chen
Zhiyin Lou
Qiong Zhang
Jian Zhao
Jian Wang
Baoguo Xiao
Intranasal LPS-mediated Parkinson's model challenges the pathogenesis of nasal cavity and environmental toxins.
PLoS ONE
author_facet Qing He
Wenbo Yu
Jianjun Wu
Chan Chen
Zhiyin Lou
Qiong Zhang
Jian Zhao
Jian Wang
Baoguo Xiao
author_sort Qing He
title Intranasal LPS-mediated Parkinson's model challenges the pathogenesis of nasal cavity and environmental toxins.
title_short Intranasal LPS-mediated Parkinson's model challenges the pathogenesis of nasal cavity and environmental toxins.
title_full Intranasal LPS-mediated Parkinson's model challenges the pathogenesis of nasal cavity and environmental toxins.
title_fullStr Intranasal LPS-mediated Parkinson's model challenges the pathogenesis of nasal cavity and environmental toxins.
title_full_unstemmed Intranasal LPS-mediated Parkinson's model challenges the pathogenesis of nasal cavity and environmental toxins.
title_sort intranasal lps-mediated parkinson's model challenges the pathogenesis of nasal cavity and environmental toxins.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2013-01-01
description Accumulating evidence implicates the relationship between neuroinflammation and pathogenesis in idiopathic Parkinson's disease (iPD). The nose has recently been considered a gate way to the brain which facilitates entry of environmental neurotoxin into the brain. Our study aims to build a PD model by a natural exposure route. In this report, we establish a new endotoxin-based PD model in mice by unilateral intranasal (i.n.) instillation of the lipopolysaccharides (LPS) every other day for 5 months. These mice display a progressive hypokinesia, selective loss of dopaminergic neurons, and reduction in striatal dopamine (DA) content, as well as α-synuclein aggregation in the SN, without systemic inflammatory and immune responses. This new PD model provides a tool for studying the inflammation-mediated chronic pathogenesis and searching for therapeutic intervention in glia-neuron pathway that will slow or halt neurodegeneration in PD.
url http://europepmc.org/articles/PMC3826714?pdf=render
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