| Literature DB >> 28168427 |
Kazimierz Gąsiorowski1, Barbara Brokos1, Valentina Echeverria2, George E Barreto3,4, Jerzy Leszek5.
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.Entities:
Keywords: Chronic inflammation; Neurodegeneration; Rage; Self-perpetuated stimulation; TLR
Mesh:
Substances:
Year: 2017 PMID: 28168427 DOI: 10.1007/s12035-017-0419-4
Source DB: PubMed Journal: Mol Neurobiol ISSN: 0893-7648 Impact factor: 5.590