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Expand All Collapse All. The Neurobiological Basis of Suicide. Other titles in this collection. Frontiers in Neuroscience. Related information. Similar articles in PubMed. Review Prevention of suicide and attempted suicide in Denmark. Epidemiological studies of suicide and intervention studies in selected risk groups.
Nordentoft M. Dan Med Bull. Prefrontal cortical thickness in depressed patients with high-risk for suicidal behavior.
J Psychiatr Res. Epub Aug 4. Bestselling Series. Harry Potter. Popular Features. New Releases. Description With recent studies using genetic, epigenetic, and other molecular and neurochemical approaches, a new era has begun in understanding pathophysiology of suicide. Emerging evidence suggests that neurobiological factors are not only critical in providing potential risk factors but also provide a promising approach to develop more effective treatment and prevention strategies.
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The Neurobiological Basis of Suicide discusses the most recent findings in suicide neurobiology. Psychological, psychosocial, and cultural factors are important in determining the risk factors for suicide; however, they offer weak prediction and can be of little clinical use.
The neurobiological basis of suicide - Ghent University Library
Interestingly, cognitive characteristics are different among depressed suicidal and depressed nonsuicidal subjects, and could be involved in the development of suicidal behavior. The characterization of the neurobiological basis of suicide is in delineating the risk factors associated with suicide. The Neurobiological Basis of Suicide focuses on how and why these neurobiological factors are crucial in the pathogenic mechanisms of suicidal behavior and how these findings can be transformed into potential therapeutic applications.
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Tuesday October 09, Transcriptional and Epigenetic Mechanisms of Depression Speaker. Our laboratory has focused on stable changes in gene expression within this circuitry that control life-long vulnerability to different forms of stress and the induction of depression-related behavioral abnormalities in mouse models. We concentrate on transcriptional pathways, deduced from large RNA-sequencing datasets of RNAs that show altered expression in several limbic brain regions of mice as a consequence of stress exposures across the life cycle. Parallel work examines transcriptional mechanisms in homologous regions in the brains of depressed humans examined postmortem.
Hypothesis and Theory ARTICLE
Current studies are exploring the detailed mechanisms by which specific transcriptional abnormalities identified in mouse models and human depression contribute to a depression-like state. We are particularly interested in how stress causes life-long changes in gene expression and hypothesize that such changes are mediated via so-called chromatin scars. We are approaching this question by studying a range of chromatin mechanisms genome-wide, including post-translational modifications of histones, DNA methylation, nucleosome positioning, and the 3-dimensional structure of chromatin.