dc.contributor.author | Gąsiorowski K. | |
dc.contributor.author | Brokos B. | |
dc.contributor.author | Echeverria V. | |
dc.contributor.author | Barreto G.E. | |
dc.contributor.author | Leszek J. | |
dc.date.accessioned | 2020-09-02T22:19:59Z | |
dc.date.available | 2020-09-02T22:19:59Z | |
dc.date.issued | 2018 | |
dc.identifier | 10.1007/s12035-017-0419-4 | |
dc.identifier.citation | 55, 2, 1463-1476 | |
dc.identifier.issn | 08937648 | |
dc.identifier.uri | https://hdl.handle.net/20.500.12728/4838 | |
dc.description | 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. © 2017, Springer Science+Business Media New York. | |
dc.language.iso | en | |
dc.publisher | Humana Press Inc. | |
dc.subject | Chronic inflammation | |
dc.subject | Neurodegeneration | |
dc.subject | Rage | |
dc.subject | Self-perpetuated stimulation | |
dc.subject | TLR | |
dc.subject | advanced glycation end product receptor | |
dc.subject | free radical | |
dc.subject | toll like receptor | |
dc.subject | advanced glycation end product receptor | |
dc.subject | toll like receptor | |
dc.subject | Alzheimer disease | |
dc.subject | brain level | |
dc.subject | chronic inflammation | |
dc.subject | chronic stress | |
dc.subject | disease course | |
dc.subject | gene amplification | |
dc.subject | human | |
dc.subject | immunoreactivity | |
dc.subject | innate immunity | |
dc.subject | nerve degeneration | |
dc.subject | protein expression | |
dc.subject | protein function | |
dc.subject | protein protein interaction | |
dc.subject | protein structure | |
dc.subject | receptor cross-talk | |
dc.subject | Review | |
dc.subject | signal transduction | |
dc.subject | animal | |
dc.subject | degenerative disease | |
dc.subject | inflammation | |
dc.subject | metabolism | |
dc.subject | nerve degeneration | |
dc.subject | physiology | |
dc.subject | Animals | |
dc.subject | Humans | |
dc.subject | Inflammation | |
dc.subject | Nerve Degeneration | |
dc.subject | Neurodegenerative Diseases | |
dc.subject | Receptor for Advanced Glycation End Products | |
dc.subject | Signal Transduction | |
dc.subject | Toll-Like Receptors | |
dc.title | RAGE-TLR Crosstalk Sustains Chronic Inflammation in Neurodegeneration | |
dc.type | Review | |