Biological basis of suicide and suicidal behavior

説明

<jats:sec><jats:title>Objective</jats:title><jats:p>Suicide is a major public health concern as each year 30000 people die by suicide in the <jats:styled-content style="fixed-case">USA</jats:styled-content> alone. In the teenage population, it is the second leading cause of death. There have been extensive studies of psychosocial factors associated with suicide and suicidal behavior. However, very little is known about the neurobiology of suicide. Recent research has provided some understanding of the neurobiology of suicide, which is the topic of this review.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Neurobiology of suicide has been studied using peripheral tissues such as platelets, lymphocytes, and cerebrospinal fluid obtained from suicidal patients or from the postmortem brains of suicide victims.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>These studies have provided encouraging information with regard to the neurobiology of suicide. They show an abnormality of the serotonergic mechanism, such as increased serotonin receptor subtypes and decreased serotonin metabolites (e.g. 5‐hydroxyindoleacetic acid). These studies also suggest abnormalities of receptor‐linked signaling mechanisms such as phosphoinositide and adenylyl cyclase. Other biological systems that appear to be dysregulated in suicide involve the hypothalamic–pituitary–adrenal axis, and neurotrophins and neurotrophin receptors. More recently, several studies have also indicated abnormalities of neuroimmune functions in suicide.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>Some encouraging information emerged from the present review, primarily related to some of the neurobiological mechanisms mentioned above. It is hoped that neurobiological studies may eventually result in the identification of appropriate biomarkers for suicidal behavior as well as appropriate therapeutic targets for its treatment.</jats:p></jats:sec>

収録刊行物

被引用文献 (1)*注記

もっと見る

詳細情報 詳細情報について

問題の指摘

ページトップへ