Inflammation and neurodegeneration : the story 'retolled'
(2012) In Trends in Pharmacological Sciences 33(10). p.51-542- 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... (More)
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.
(Less)
- author
- Drouin-Ouellet, Janelle LU and Cicchetti, Francesca
- publishing date
- 2012-10
- type
- Contribution to journal
- publication status
- published
- keywords
- Alzheimer Disease, Animals, Humans, Immunity, Innate, Inflammation, Parkinson Disease, Signal Transduction, Toll-Like Receptors, Journal Article, Research Support, Non-U.S. Gov't, Review
- in
- Trends in Pharmacological Sciences
- volume
- 33
- issue
- 10
- pages
- 10 pages
- publisher
- Elsevier
- external identifiers
-
- scopus:84866734401
- pmid:22944460
- ISSN
- 0165-6147
- DOI
- 10.1016/j.tips.2012.07.002
- language
- English
- LU publication?
- no
- id
- 78488115-5529-47a1-8506-012b5b543bc8
- date added to LUP
- 2016-11-22 09:04:29
- date last changed
- 2024-05-03 14:13:13
@article{78488115-5529-47a1-8506-012b5b543bc8,
abstract = {{<p>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.</p>}},
author = {{Drouin-Ouellet, Janelle and Cicchetti, Francesca}},
issn = {{0165-6147}},
keywords = {{Alzheimer Disease; Animals; Humans; Immunity, Innate; Inflammation; Parkinson Disease; Signal Transduction; Toll-Like Receptors; Journal Article; Research Support, Non-U.S. Gov't; Review}},
language = {{eng}},
number = {{10}},
pages = {{51--542}},
publisher = {{Elsevier}},
series = {{Trends in Pharmacological Sciences}},
title = {{Inflammation and neurodegeneration : the story 'retolled'}},
url = {{http://dx.doi.org/10.1016/j.tips.2012.07.002}},
doi = {{10.1016/j.tips.2012.07.002}},
volume = {{33}},
year = {{2012}},
}