PSYCHIATRIE AUS NATURWISSENSCHAFTLICHER SICHT

Bei der Suche nach den Ursachen psychischer Erkrankungen dominierten bis zum Beginn des 20. Jahrhunderts dualistische Vorstellungen, wonach „geistige Umnachtung“ oder „Wahnsinn“ aus der Sicht moralisierender Theorien häufig als Folge sittlichen Fehlverhaltens angesehen wurde oder aber gänzlich unerklärbar erschien. Die Entdeckung der hirnorganischen Substrate der motorischen Aphasie (Sprachunfähigkeit) und des Stirnhirnsyndroms, das mit einem Verlust differenzierter Persönlichkeitsmerkmale einhergeht, sowie die Beschreibung der hirnpathologischen Grundlagen der Alzheimer-Krankheit und der progressiven Paralyse führten etwa ab 1900 zu einer zunehmenden Akzeptanz hirnbiologischer Sichtweisen psychischer Störungen. Seit Einführung des ersten Antipsychotikums im Jahre 1952 und des ersten Antidepressivums im Jahre 1957 haben sich die Behandlungsmöglickeiten fast aller psychiatrischen Krankheitsbilder ganz erheblich verbessert. In den letzten zwanzig Jahren konnten hirnbiologische Korrelate schizophrener Erkrankungen nachgewiesen werden, die die Pathophysiologie dieser bislang rätselhaften Erkrankung verständlicher machen. In der Therapie aller psychischer Störungen werden die besten Erfolge dann erreicht, wenn hirnbiologische und psychotherapeutische Methoden integrativ angewandt werden. Aus klinisch-praktischer Sicht ist davon auszugehen, dass beides an letztlich identischen intrazerebralen/innerpsychischen Mechanismen wirksam ist

SONDERFORSCHUNGSBEREICH 426 „LIMBISCHE STRUKTUREN UND FUNKTIONEN“ IM ZENTRUM DES GEHIRNS

An das „Limbische System“ knüpfen viele jener ungelösten Fragen an, die von jeher als zentral für das Verständnis von Funktion und Dysfunktion des menschlichen Gehirns betrachtet werden. Hier sind molekularzelluläre Eigenschaften, lokale Organisationsformen, Systemfunktionen, die menschliche Empfindung und das Gedächtnis auf vielfältigste Art miteinander verknüpft, zu deren Erfassung interaktive und multidisziplinäre wissenschaftliche Ansätze mit unterschiedlichen Ebenen der Analyse in besonderer Weise geeignet sind

Neuroanatomical correlates of aggressiveness: a case-control voxel- and surface-based morphometric study

Aggression occurs across the population ranging on a symptom continuum. Most previous studies have used magnetic resonance imaging in clinical/forensic samples, which is associated with several confounding factors. The present study examined structural brain characteristics in two healthy samples differing only in their propensity for aggressive behavior. Voxel- and surface-based morphometry (SBM) analyses were performed on 29 male martial artists and 32 age-matched male controls. Martial artists had significantly increased mean gray matter volume in two frontal (left superior frontal gyrus and bilateral anterior cingulate cortex) and one parietal (bilateral posterior cingulate gyrus and precuneus) brain clusters compared to controls (whole brain: p < 0.001, cluster level: family-wise error (FWE)-corrected). SBM analyses revealed a trend for greater gyrification indices in martial artists compared to controls in the left lateral orbital frontal cortex and the left pars orbitalis (whole brain: p < 0.001, cluster level: FWE-corrected). The results indicate brain structural differences between martial artists and controls in frontal and parietal brain areas critical for emotion processing/inhibition of emotions as well as empathic processes. The present study highlights the importance of studying healthy subjects with a propensity for aggressive behavior in future structural MRI research on aggression

Os possíveis papéis da S100B na esquizofrenia

BACKGROUND: Scientific evidence for increased S100B concentrations in the peripheral blood of acutely ill schizophrenia patients is consistent. In the past, this finding was mainly considered to reflect astroglial or blood-brain barrier dysfunction. METHODS: Using Entrez, PubMed was searched for articles published on or before June 15, 2011, including electronic early release publications, in order to determine other potential links between S100B and current hypotheses for schizophrenia. RESULTS: S100B is potentially associated with the dopamine and glutamate hypotheses. Supporting the glial hypothesis, an increased expression of S100B has been detected in cortical astrocytes of paranoid schizophrenia cases, while decreased oligodendrocytic expression has been observed in residual schizophrenia. Recently, the neuroinflammation hypothesis of schizophrenia has gained attention. S100B may act as a cytokine after secretion from glial cells, CD8+ lymphocytes and NK cells, activating monocytes and microglial cells. Moreover, S100B exhibits adipokine-like properties and may be dysregulated in schizophrenia due to disturbances in insulin signaling, leading to the increased release of S100B and free fatty acids from adipose tissue. DISCUSSION: Dysregulation of pathways related to S100B appears to play a role in schizophrenia. However, S100B is expressed in different cell types and is involved in many regulatory processes. Currently, "the most important" mechanism related to schizophrenia cannot be determined.CONTEXTO: Evidências científicas do aumento da concentração da proteína S100B no sangue de pacientes esquizofrênicos são muito consistentes. No passado essa informação era principalmente considerada como reflexo da disfunção astroglial ou da barreira hematoencefálica. MÉTODOS: Pesquisa de publicações no PubMed até o dia 15 de junho de 2011 visando estabelecer potenciais ligações entre a proteína S100B e as hipóteses correntes da esquizofrenia. RESULTADOS: A S100B está potencialmente associada com as hipóteses dopaminérgica e glutamatérgica. O aumento da expressão de S100B tem sido detectado em astrócitos corticais em casos de esquizofrenia paranoide, enquanto se observa uma redução da expressão em oligodendrócitos na esquizofrenia residual, dando suporte à hipótese glial. Recentemente, a hipótese da neuroinflamação da esquizofrenia tem recebido atenção crescente. Nesse sentido, a S100B pode funcionar como uma citocina secretada por células gliais, linfócitos CD8+ e células NK, levando à ativação de monócitos e microglia. Além disso, a S100B apresenta propriedades do tipo adipocina e pode estar desregulada na esquizofrenia, devido a distúrbios da sinalização de insulina, levando ao aumento da liberação de S100B e ácidos graxos do tecido adiposo. CONCLUSÃO: A expressão de S100B em diferentes tipos celulares está envolvida em muitos processos regulatórios. Atualmente, não pode ser respondido qual mecanismo relacionado à esquizofrenia é o mais importante