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Neurobiology of Suicide

Childhood adversity is associated with greater risk for depression in adulthood, aggressive traits and suicide.

The biological basis of this relationship is mostly unknown, though epigenetic effects mediating less expression of the glucocorticoid receptor (GR) gene in suicidal individuals who report childhood adversity have been suggested.

Arrango Research Team

Arango Research Team

Stress and suicide are also associated with having fewer neurons in parts of the brain and nerve process shrinkage in the prefrontal cortex(PFC) and hippocampus (HC). Smaller HC volume may constitute a risk factor forstress-related psychopathology.

In addition, we often find that depressed individuals who commit suicide show lower serotonin transporter (5-HTT) and higher serotonin 1A receptor (5-HT1A) binding in the PFC and a higher rate of childhood adverse events. We hypothesize that this neurobiological phenotype may result from a combination of genes, environment and epigenetic effects.

The Brain and Childhood Adversity and the Link to Suicide

We aim to determine whether serotonin receptor (5-HT1A) binding, the brain growth factor BDNF, measures of the hypothalamus-pituitary-adrenocortical (HPA) stress-response axis and candidate gene expression and epigenetic effects, correlate with neuron density or number in the PFC and HC in 5 groups of age- and sex-matched depressed suicides; nonpsychiatric controls with and without reported childhood adversity; and depressed individuals with no history of suicide attempts, postmortem.

We aim to

  • determine the effect of childhood adversity on various regions of the brain, including the dorsal PFC, anterior cingulate cortex (ACC), and HC,
  • determine the effect of childhood adversity on neuronal gene expression and methylation levels of candidate genes in these brain regions in the five groups,
  • separate the relationship of depression from that of suicide to brain biology including neuron, glia and BDNF-IR cell density and
  • test the relationship between lifetime aggression and childhood adversity, neuron and glia number or density, serotonin indices, HPA axis indices, gene expression and methylation.