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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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 |
work_keys_str_mv |
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