Inflammation and neurodegeneration: the story 'retolled'.
Identifieur interne : 000A21 ( PubMed/Curation ); précédent : 000A20; suivant : 000A22Inflammation and neurodegeneration: the story 'retolled'.
Auteurs : Janelle Drouin-Ouellet [Canada] ; Francesca CicchettiSource :
- Trends in pharmacological sciences [ 1873-3735 ] ; 2012.
English descriptors
- KwdEn :
- Alzheimer Disease (immunology), Alzheimer Disease (metabolism), Animals, Humans, Immunity, Innate, Inflammation (immunology), Inflammation (metabolism), Parkinson Disease (genetics), Parkinson Disease (immunology), Parkinson Disease (metabolism), Signal Transduction, Toll-Like Receptors (metabolism).
- MESH :
- chemical , metabolism : Toll-Like Receptors.
- genetics : Parkinson Disease.
- immunology : Alzheimer Disease, Inflammation, Parkinson Disease.
- metabolism : Alzheimer Disease, Inflammation, Parkinson Disease.
- Animals, Humans, Immunity, Innate, Signal Transduction.
Abstract
Toll-like receptors (TLRs) play a crucial role in innate immunity by recognizing conserved motifs predominantly found in microorganisms. Increasing evidence supports a role for TLRs in sterile inflammation as observed in neurodegenerative disorders. This includes work suggesting a contribution for these receptors to the pathophysiology of Alzheimer's disease (AD), Parkinson's disease (PD), and related disorders. In this review, the potential role of TLRs in the context of protein aggregation, neuronal degeneration, and genetic risk factors is addressed. In particular, we discuss the evidence derived from experimental models of both AD and PD which suggests that activation of TLRs can have beneficial and detrimental effects on pathological features such as protein aggregation and neuronal death. A deeper understanding of these dichotomous observations could be used for therapeutic benefit.
DOI: 10.1016/j.tips.2012.07.002
PubMed: 22944460
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pubmed:22944460Le document en format XML
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<author><name sortKey="Drouin Ouellet, Janelle" sort="Drouin Ouellet, Janelle" uniqKey="Drouin Ouellet J" first="Janelle" last="Drouin-Ouellet">Janelle Drouin-Ouellet</name>
<affiliation wicri:level="1"><nlm:affiliation>Axe Neurosciences, Centre de Recherche du CHUL, Québec, QC, G1V 4G2, Canada. janelle.drouin-ouellet@crchul.ulaval.ca</nlm:affiliation>
<country xml:lang="fr">Canada</country>
<wicri:regionArea>Axe Neurosciences, Centre de Recherche du CHUL, Québec, QC, G1V 4G2</wicri:regionArea>
</affiliation>
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<author><name sortKey="Cicchetti, Francesca" sort="Cicchetti, Francesca" uniqKey="Cicchetti F" first="Francesca" last="Cicchetti">Francesca Cicchetti</name>
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<term>Humans</term>
<term>Immunity, Innate</term>
<term>Inflammation (immunology)</term>
<term>Inflammation (metabolism)</term>
<term>Parkinson Disease (genetics)</term>
<term>Parkinson Disease (immunology)</term>
<term>Parkinson Disease (metabolism)</term>
<term>Signal Transduction</term>
<term>Toll-Like Receptors (metabolism)</term>
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<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Toll-Like Receptors</term>
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<front><div type="abstract" xml:lang="en">Toll-like receptors (TLRs) play a crucial role in innate immunity by recognizing conserved motifs predominantly found in microorganisms. Increasing evidence supports a role for TLRs in sterile inflammation as observed in neurodegenerative disorders. This includes work suggesting a contribution for these receptors to the pathophysiology of Alzheimer's disease (AD), Parkinson's disease (PD), and related disorders. In this review, the potential role of TLRs in the context of protein aggregation, neuronal degeneration, and genetic risk factors is addressed. In particular, we discuss the evidence derived from experimental models of both AD and PD which suggests that activation of TLRs can have beneficial and detrimental effects on pathological features such as protein aggregation and neuronal death. A deeper understanding of these dichotomous observations could be used for therapeutic benefit.</div>
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<CopyrightInformation>Copyright © 2012 Elsevier Ltd. All rights reserved.</CopyrightInformation>
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