Debate aspects of suicidology: the relationship of neuroinflammatory with suicidal behavior in mentally healthy people. Part I

A large body of literature has been accumulated, which proves that suicidal behavior (completed suicides) is induced by inflammation of the peripheral and central nervous system, which is realized as a result of congenital gene polymorphisms and/or changes in epigenomic marks. The purpose of the work is to systematize information about the role of cytokines and inflammatory chemokines in the processes of translation of genomic defects into suicidal behavior in mentally healthy people. The work examines the pathophysiology of neuroinflammation, provides molecular and cytological information that forms a natural scientific understanding of the differences between neuroinflammation with the participation of microglia, cytoand chemokines and classical inflammation with the activation of peripheral macrophages, T-cells, and eicosotetraenoic acid products. The role of the kynurenine pathway and NMDA receptors in the formation of neuroinflammation and suicidal behavior is discussed. Shows how peripheral inflammation can induce neuroinflammation. The pathophysiology of the formation of suicidal behavior is considered using examples of the connection between neuroinflammation and its manifestations (suicidal thoughts, suicide attempts and completed suicides) in individuals without mental disorders.