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Does Infection-Induced Immune Activation Contribute to Dementia?
Author(s) -
Tatiana Barichello,
Jaqueline S. Generoso,
Jéssica A. Goularte,
Allan Collodel,
Meagan R. Pitcher,
Lutiana R. Simões,
João Quevedo,
Felipe DalPizzol
Publication year - 2015
Publication title -
aging and disease
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 1.808
H-Index - 54
ISSN - 2152-5250
DOI - 10.14336/ad.2015.0521
Subject(s) - receptor , damp , pattern recognition receptor , innate immune system , immune system , rage (emotion) , immune receptor , biology , immunology , pathogen associated molecular pattern , microglia , microbiology and biotechnology , inflammation , neuroscience , biochemistry , physics , meteorology
The central nervous system (CNS) is protected by a complex blood-brain barrier system; however, a broad diversity of virus, bacteria, fungi, and protozoa can gain access and cause illness. As pathogens replicate, they release molecules that can be recognized by innate immune cells. These molecules are pathogen-associated molecular patterns (PAMP) and they are identified by pattern-recognition receptors (PRR) expressed on antigen-presenting cells. Examples of PRR include toll-like receptors (TLR), receptors for advanced glycation endproducts (RAGE), nucleotide binding oligomerisation domain (NOD)-like receptors (NLR), c-type lectin receptors (CLR), RIG-I-like receptors (RLR), and intra-cytosolic DNA sensors. The reciprocal action between PAMP and PRR triggers the release of inflammatory mediators that regulate the elimination of invasive pathogens. Damage-associated molecular patterns (DAMP) are endogenous constituents released from damaged cells that also have the ability to activate the innate immune response. An increase of RAGE expression levels on neurons, astrocytes, microglia, and endothelial cells could be responsible for the accumulation of αβ-amyloid in dementia and related to the chronic inflammatory state that is found in neurodegenerative disorders.

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