Chronic inflammatory processes within the central nervous system (CNS) are in part
responsible for the development of neurodegenerative and psychiatric diseases. These processes are
associated with, among other things, the increased and disturbed activation of microglia and the
elevated production of proinflammatory factors. Recent studies indicated that the disruption of the
process of resolution of inflammation (RoI) may be the cause of CNS disorders. It is shown that the
RoI is regulated by endogenous molecules called specialized pro-resolving mediators (SPMs),
which interact with specific membrane receptors. Some SPMs activate formyl peptide receptors
(FPRs), which belong to the family of seven-transmembrane G protein-coupled receptors. These
receptors take part not only in the proinflammatory response but also in the resolution of the inflammation
process. Therefore, the activation of FPRs might have complex consequences.
This review discusses the potential role of FPRs, and in particular the role of FPR2 subtype, in the
brain under physiological and pathological conditions and their involvement in processes underlying
neurodegenerative and psychiatric disorders as well as ischemia, the pathogenesis of which
involves the dysfunction of inflammatory processes.
Keywords: Neuroinflammation, glial cells, resolution of inflammation, formyl peptide receptors, new pro-resolving agonists,
Alzheimer's disease, depression, ischemia.
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