RAGE-TLR Crosstalk Sustains Chronic Inflammation in Neurodegeneration

Kazimierz Gąsiorowski; Barbara Brokos; Valentina Echeverria; George E. Barreto; Jerzy Leszek

doi:10.1007/s12035-017-0419-4

RAGE-TLR Crosstalk Sustains Chronic Inflammation in Neurodegeneration

Kazimierz Gąsiorowski, Barbara Brokos, Valentina Echeverria, George E. Barreto, Jerzy Leszek

Research output: Contribution to journal › Review article › peer-review

Abstract

Chronic inflammatory reactions are consistenly present in neurodegeneration of Alzheimer type and are considered important factors that accelerate progression of the disease. Receptors of innate immunity participate in triggering and driving inflammatory reactions. For example, Toll-like receptors (TLRs) and receptor for advanced glycation end product (RAGE), major receptors of innate immunity, play a central role in perpetuation of inflammation. RAGE activation should be perceived as a primary mechanism which determines self-perpetuated chronic inflammation, and RAGE cooperation with TLRs amplifies inflammatory signaling. In this review, we highlight and discuss that RAGE-TLR crosstalk emerges as an important driving force of chronic inflammation in Alzheimer’s disease.

Original language	English
Pages (from-to)	1463-1476
Number of pages	14
Journal	Molecular Neurobiology
Volume	55
Issue number	2
DOIs	https://doi.org/10.1007/s12035-017-0419-4
Publication status	Published - 1 Feb 2018
Externally published	Yes

Keywords

Chronic inflammation
Neurodegeneration
Rage
Self-perpetuated stimulation
TLR

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10.1007/s12035-017-0419-4

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abstract = "Chronic inflammatory reactions are consistenly present in neurodegeneration of Alzheimer type and are considered important factors that accelerate progression of the disease. Receptors of innate immunity participate in triggering and driving inflammatory reactions. For example, Toll-like receptors (TLRs) and receptor for advanced glycation end product (RAGE), major receptors of innate immunity, play a central role in perpetuation of inflammation. RAGE activation should be perceived as a primary mechanism which determines self-perpetuated chronic inflammation, and RAGE cooperation with TLRs amplifies inflammatory signaling. In this review, we highlight and discuss that RAGE-TLR crosstalk emerges as an important driving force of chronic inflammation in Alzheimer{\textquoteright}s disease.",

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AU - Echeverria, Valentina

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AU - Leszek, Jerzy

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AB - Chronic inflammatory reactions are consistenly present in neurodegeneration of Alzheimer type and are considered important factors that accelerate progression of the disease. Receptors of innate immunity participate in triggering and driving inflammatory reactions. For example, Toll-like receptors (TLRs) and receptor for advanced glycation end product (RAGE), major receptors of innate immunity, play a central role in perpetuation of inflammation. RAGE activation should be perceived as a primary mechanism which determines self-perpetuated chronic inflammation, and RAGE cooperation with TLRs amplifies inflammatory signaling. In this review, we highlight and discuss that RAGE-TLR crosstalk emerges as an important driving force of chronic inflammation in Alzheimer’s disease.

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RAGE-TLR Crosstalk Sustains Chronic Inflammation in Neurodegeneration

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Keywords

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