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Toll-Like Receptors in Neurodegeneration

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Toll-like Receptors: Roles in Infection and Neuropathology

Part of the book series: Current Topics in Microbiology and Immunology ((CT MICROBIOLOGY,volume 336))

Abstract

Innate pattern recognition receptors are implicated in first-line defense against pathogens but also participate in maintenance of tissue homeostasis and response to injury. This chapter reviews the role of Toll-like receptors (TLRs) in neuronal and glial responses that are associated with neurodegeneration. Accompanying roles for infection and inflammation, involvement in clinical neurodegenerative disorders, and heterogeneity of glial response are discussed. A “strength of signal” hypothesis is advanced in an attempt to reconcile evolutionarily selected and therefore likely beneficial effects of TLR signaling in the nervous system with capability for neurotoxocity and gliotoxicity.

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Abbreviations

AD:

Alzheimer’s disease

CNS:

Central nervous system

CpG:

Cytosine-phosphate-guanine

dsRNA:

Double-stranded RNA

EAE:

Experimental autoimmune encephalomyelitis

HIV:

Human immunodeficiency virus

HSP:

Heat-shock protein

iNOS:

Inducible nitric oxide synthase

LPS:

Lipopolysaccharide

MyD88:

Myeloid differentiation primary response gene (88)

NF-κB:

Nuclear factor kappa B

NO:

Nitric oxide

NPC:

Niemann–Pick type C

SIGIRR:

Single immunoglobulin IL-1R-related molecule

STAT:

Signal transducer and activator of transcription

TLR:

Toll-like receptor

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Acknowledgments

Research in my laboratory is supported by Scleroseforeningen, Novo Nordisk Fonden, Lundbeckfonden and The Danish Agency for Research and Innovation. I acknowledge the EU/ESF COST Action BM0603 “Neurinfnet” for its support of collaborative interactions that contributed to this review.

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Correspondence to Trevor Owens .

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Owens, T. (2009). Toll-Like Receptors in Neurodegeneration. In: Kielian, T. (eds) Toll-like Receptors: Roles in Infection and Neuropathology. Current Topics in Microbiology and Immunology, vol 336. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-00549-7_6

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