Glial Markers of Suicidal Behavior in the Human Brain-A Systematic Review of Postmortem Studies

Suicide is a major public health priority, and its molecular mechanisms appear to be related to glial abnormalities and specific transcriptional changes. This study aimed to identify and synthesize evidence of the relationship between glial dysfunction and suicidal behavior to understand the neurobi...

Full description

Saved in:
Bibliographic Details
Published inInternational journal of molecular sciences Vol. 25; no. 11; p. 5750
Main Authors Yamamoto, Mana, Sakai, Mai, Yu, Zhiqian, Nakanishi, Miharu, Yoshii, Hatsumi
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 01.06.2024
MDPI
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Suicide is a major public health priority, and its molecular mechanisms appear to be related to glial abnormalities and specific transcriptional changes. This study aimed to identify and synthesize evidence of the relationship between glial dysfunction and suicidal behavior to understand the neurobiology of suicide. As of 26 January 2024, 46 articles that met the inclusion criteria were identified by searching PubMed and ISI Web of Science. Most postmortem studies, including 30 brain regions, have determined no density or number of total Nissl-glial cell changes in suicidal patients with major psychiatric disorders. There were 17 astrocytic, 14 microglial, and 9 oligodendroglial studies using specific markers of each glial cell and further on their specific gene expression. Those studies suggest that astrocytic and oligodendroglial cells lost but activated microglia in suicides with affective disorder, bipolar disorders, major depression disorders, or schizophrenia in comparison with non-suicided patients and non-psychiatric controls. Although the data from previous studies remain complex and cannot fully explain the effects of glial cell dysfunction related to suicidal behaviors, they provide risk directions potentially leading to suicide prevention.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Undefined-1
ObjectType-Feature-3
ObjectType-Review-4
content type line 23
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms25115750