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Objective

Parasuicidal and self-harm behavior are debilitating symptoms affecting both mood disorder and personality disorder patients. Previous publications suggest that a complex interaction between genetic predisposition and acquired environmental factors are causing parasuicidal behavior [1, 2]. Pro-inflammatory cytokines have made a recent comeback in neuroscience [3]. Post-mortem brain data has shown increased expression patterns of these proinflammatory cytokines but also of a protein-family that precedes and mediates their production: the toll-like receptor family (TLR). TLR-3 in particular is an interesting candidate in the context of psychiatric research since it is expressed in neurons and since its increased expression in the prefrontal cortex has been associated with suicide [4]. The neuroinflammation hypothesis revolves around the debate whether these findings reflect the cause of a phenotype (trait) or whether it is a reaction to a concomitant disease process (state). When studying parasuicidal behavior one is confronted with a similar problem, is parasuicidal behavior a trait and depends on the individual or is it a state independent of the genetic predisposition of the individual? The hypothesis of the present study is that genetic polymorphisms of the TLR-3 correlate with the phenotype self-harm within a sample of affective disorder patients.