Is there a difference between microglial activation in the human brain between individuals, who have committed suicide and the control group?

Suicide is a deliberate act of the intentional self-inflicted death. Neuroinflammation is suggested to be linked to suicide. Microglia – a cell of the innate immune system of the central nervous system (CNS) – is known to release cytokines that can modulate noradrenergic or serotonergic neurotransmission in the cortex leading to individual’s suicidality. The aim of this study was to find out if there is any difference between microglial activation in three different CNS regions between individuals, who had committed suicide and the control group. Post-mortem human brain tissues were obtained from seven individuals, who had committed suicide (median age 26±7.2 years) and from eight individuals (control group), who died from other causes (median age 29.5±6.0 years). Quantitative analysis of activated microglia/macrophages location in the white and gray matter of prefrontal cortex, striatum and substantia nigra was done using immunohistochemical staining with a marker CD68. Statistical analysis was done by SPSS 26. Significantly more diffuse CD68 positive (CD68+) cells were found in the white matter of prefrontal cortex compared to its gray matter (p=0.005). The number of CD68+ cells found in all three regions both white and gray matter of the brain did not differ between both groups - controls and suicides. However, CD68 positivity was different between brain regions, where only none to few CD68+ cells per visual field were found in the striatum, but significantly more CD68+ cells were found in the substantia nigra compared to prefrontal cortex (p=0.001) taking into account white and gray matter. As this study could not confirm increased number of CD68+ cells in individuals, who had committed suicide, it suggests that different inflammation pathways could be involved. Interestingly, we found that comparing three different brain regions substantia nigra had the most CD68+ cells.