Thesis (M.S.) -- University of Texas Southwestern Medical Center at Dallas, 2006. / Vita. Bibliography: pp.40-43.

Thesis (M.S.) -- University of Texas Southwestern Medical Center at Dallas, 2006. / Vita. Bibliography: pp. 159-175.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2007. / Härtill 4 uppsatser.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2009.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2006. / Härtill 5 uppsatser.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2010.

Representing a major public health concern, suicide is a leading cause of death worldwide. Generally regarded as a behavior with a multitude of state and trait dependent risk factors (e.g. psychiatric disorders, substance abuse, genetics), explanations as to why certain individuals commit suicide while others do not are complex. Of interest is in studying potential trait dependent variables involved in the neurobiology of suicide, particularly at the cellular level. Knowledge of the cellular integrity may aid in explaining the observed macroscopic alterations and ultimately the behavioral correlates associated with suicidality. Therefore we set out to summarize extant knowledge of the cellular alterations occurring in the brains of major depressive and suicide individuals. Following this, we conducted our own cellular investigation in a region known to be altered in major depression and suicide, a supracallosal area of BA24a. Neuronal and glial cell densities as well as neuronal cell sizes were assessed in upper and lower cortical layers between sudden-death controls and MDD suicide subjects. Secondary analyses were also conducted to examine the effect of alcohol on depressed suicides. Analyses of cell densities and neuronal soma sizes between controls and MDD suicide subjects did not reveal any significant differences. Further analyses showed increased glial cell densities in alcoholic depressed suicides. Future studies are necessary to examine explicit changes in the cellular compositions occurring in alcoholic dependent individuals. Staining techniques aimed at targeting specific subtypes of neurons and glial cells will help determine if these cell populations do in fact have an influential role in suicide and MDD.

One of the most difficult and serious challenges facing the mental health professional is the prevention of suicide. Efficient prevention, however, depends on early detection of patients at risk for suicidal behaviour, which in turn depends on a better understanding of the predisposing factors. Over the last years, based on a large volume of data, it has become increasingly clear that subjects who commit suicide present high levels of impulsive and impulsive-aggressive behaviours. / In the first approach, we investigate whether levels of the impulsive aggressive diathesis were more important in suicide occurring at different life stages. In the second, we investigate whether levels of the diathesis predicted when during the course of major depressive disorder suicide occurs. / Family studies have consistently indicated that suicidal behaviour tends to cluster in families. However, relatives also present increased risk for psychiatric morbidity, and therefore, the critical question is whether or not the liability to suicidal behavior is given by the same predisposition to the coexistent psychiatric disorders. / Therefore, in the third study, we examined the independence of familial liability using a three group design. The relatives of deceased suicide probands who died in the context of a major depressive episode are compared to the relatives of living depressed subjects without a history of suicide and to the relatives of healthy controls screened for the absence of major depression and suicide.

Dissertation (Ph.D.) -- University of Texas Southwestern Medical Center at Dallas, 2008. / Vita. Bibliography: p. 149-167.

Thesis (M.S.)--University of Michigan, 2002. / eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 32-36).