Inflammation and neurodegeneration: the story 'retolled'.
Identifieur interne : 001203 ( Main/Exploration ); précédent : 001202; suivant : 001204Inflammation 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
Affiliations:
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Le document en format XML
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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></front></TEI><affiliations><list><country><li>Canada</li></country></list><tree><noCountry><name sortKey="Cicchetti, Francesca" sort="Cicchetti, Francesca" uniqKey="Cicchetti F" first="Francesca" last="Cicchetti">Francesca Cicchetti</name></noCountry><country name="Canada"><noRegion><name sortKey="Drouin Ouellet, Janelle" sort="Drouin Ouellet, Janelle" uniqKey="Drouin Ouellet J" first="Janelle" last="Drouin-Ouellet">Janelle Drouin-Ouellet</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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