{"id":14830,"date":"2023-11-15T09:48:31","date_gmt":"2023-11-15T14:48:31","guid":{"rendered":"https:\/\/sciencebeta.com\/?p=14830"},"modified":"2023-11-15T09:48:31","modified_gmt":"2023-11-15T14:48:31","slug":"suicide-risk-brain-inflammation","status":"publish","type":"post","link":"https:\/\/sciencebeta.com\/suicide-risk-brain-inflammation\/","title":{"rendered":"Suicide Risk Linked to Brain Inflammation, Loss of Protective Mechanisms"},"content":{"rendered":"

In a first-of-its-kind study, researchers found that lost brain protection systems and overactive inflammation<\/a> may contribute to the risk of suicide. The results provide additional justification for investigating the potential of anti-inflammatory drugs as a preventive measure, particularly in scenarios of early suicidal ideation detection.<\/p>\n

“As\u00a0suicide rates\u00a0continue to rise, we must develop additional evidence-based strategies to address all the factors that contribute to suicide risk. Our study pinpoints several key changes in the\u00a0brain\u00a0that one day could be targeted for treatment with the goal of reducing risk and saving lives,”<\/p><\/blockquote>\n

said the Van Andel Institute’s Lena Brundin, M.D., Ph.D., leader of the study. Columbia University Department of Psychiatry’s J. John Mann, M.D., and Western Michigan University Homer Stryker M.D. School of Medicine’s Eric Achtyes, M.D., M.S. also co-led the study.<\/p>\n

Finding Key Molecular Differences<\/h2>\n

A combination of psychological, social, and biological variables contribute to suicidal behavior. Previous research, including results by Brundin, Mann, and Achtyes, suggests that chronic inflammation may generate a toxic imbalance that affects brain chemistry and increases the risk of suicide.<\/p>\n

The new findings expand on previous research by identifying key molecular differences that drive inflammation and may contribute to suicidal behavior.<\/p>\n

\"Differentially<\/a>
Differentially expressed genes in temporal cortical brain tissue from suicidal decedents versus nonsuicide, nonpsychiatric controls. N for healthy\u2009=\u200932; N for suicide decedent\u2009=\u200929. Lines in the notched boxplots showing 25, 75 percentiles and medians. A Normalized counts per million (CPM) of ENSG00000249743; B CPM of NPAS4; C CPM of MT-NRN1. P-values were adjusted by applying the Benjamini-Hochberg method to control false discovery rate (FDR). Credit: Molecular Psychiatry (2023). DOI: 10.1038\/s41380-023-02311-9<\/figcaption><\/figure>\n

The brains of 29 persons who died by suicide were compared to the brains of 32 people who died from other causes by the research team. The study’s suicide victims were mostly free of antidepressant and antipsychotic medicines, allowing the researchers to observe suicide-related molecular changes that would otherwise be hidden.<\/p>\n

“Our goal is to prevent suicide by better understanding the\u00a0brain function\u00a0associated with it. We focused on the brain because that’s where the\u00a0biological processes\u00a0that affect mood,\u00a0suicidal ideation\u00a0and intent, and decision-making reside. This study enabled us to see the brain at the moment of greatest risk and pinpoint biological markers of that risk,”<\/p><\/blockquote>\n

Mann said.<\/p>\n

Gene Methylation and Transcriptomics<\/h2>\n

Overall, the researchers discovered increased inflammation as well as decreased activation in brain-protection pathways. Specific changes in the brains of suicide victims include:<\/p>\n