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Psychische Erkrankungen in der Lebensspanne ... - DGPPN

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Topic 4 G Affektive Störungen, F3 // Affective disor<strong>der</strong>s, F3<br />

002<br />

Psychoanalytische Behandlung <strong>der</strong> chronischen Depression und<br />

ihre neuronalen Korrelate: E<strong>in</strong>e Verlaufstudie mit <strong>der</strong> fMRT<br />

Henrik Kessler (Universitätskl<strong>in</strong>ik Ulm, Kl<strong>in</strong>ik für Psychosomatik)<br />

003<br />

Treatment-resistant depression (TRD): current pharmacological<br />

treatment options<br />

Mazda Adli (Charité Campus Mitte, Psychiatrie und Psychotherapie,<br />

Berl<strong>in</strong>)<br />

Although the neurobiological basis of depression is far from be<strong>in</strong>g<br />

sufficiently un<strong>der</strong>stood thorough consi<strong>der</strong>able progress has been<br />

achieved <strong>in</strong> the recent years to un<strong>der</strong>stand important mechanisms<br />

on genetic, endocr<strong>in</strong>ological and cellular levels which open up potential<br />

novel and more specific treatment approaches. However,<br />

today strategies for the treatment of depression comprise a confus<strong>in</strong>g<br />

variety of options. About 30 antidepressants are currently on<br />

the market which ma<strong>in</strong>ly differ with regard to their side effect profiles.<br />

All biological treatment strategies (except for sleep deprivation)<br />

show a latency of onset of several weeks and a non-response<br />

rate of about 30 to 50 %. Therefore, <strong>in</strong> daily rout<strong>in</strong>e it has been<br />

shown useful to follow a stepwise sequence of therapeutic strategies<br />

and to perform a standardized evaluation of response at critical decision<br />

po<strong>in</strong>ts to avoid or to overcome TRD. Innovative pharmacological<br />

and personalized treatment approaches carry the promise of<br />

shorten<strong>in</strong>g treatment duration and <strong>in</strong>creas<strong>in</strong>g response rates <strong>in</strong> the<br />

near future. As of today, depressive disor<strong>der</strong>s show a good prognosis<br />

if the treatment options cover all available strategies and the response<br />

to a particular treatment is evaluated based on systematic<br />

treatment algorithms.<br />

004<br />

Deep Bra<strong>in</strong> Stimulation as a putative treatment for treatment-<br />

resistant depression<br />

Thomas Schläpfer (Universitätskl<strong>in</strong>ikum Bonn, Psychiatrie und Psychotherapie)<br />

Introduction: A substantial number of patients suffer<strong>in</strong>g from severe<br />

neuropsychiatric disor<strong>der</strong>s do not respond to conventional<br />

therapeutic approaches. Results from functional neuroimag<strong>in</strong>g research<br />

and the development of neuromodulatory treatments lead to<br />

novel putative strategies.<br />

Method: Recently, one of those methods, deep bra<strong>in</strong> stimulation<br />

(DBS) has been applied <strong>in</strong> selected patient with major depression<br />

and obsessive-compulsive disor<strong>der</strong> and major depression.<br />

Discussion / Results: Different targets have been chosen <strong>in</strong> a hypothesis-guided<br />

way and first results have demonstrated that DBS<br />

might be able to modulate dysfunctional neural networks <strong>in</strong> both<br />

major depression and OCD. Although DBS is a unique and promis<strong>in</strong>g<br />

method for otherwise treatment resistant psychiatric patients,<br />

mandatory treatment standards have to be applied for patient and<br />

target selection.<br />

122<br />

Donnerstag, 26. 11. 2009, 08.30 – 10.00 Uhr, Saal 7<br />

S-037 Symposium<br />

Genetic predisposition and stressors – who will become depressed?<br />

(Referat Neurobiologie und Genetik)<br />

Vorsitz: H. Grabe (Stralsund), M. Rietschel (Mannheim)<br />

001<br />

Depression and Genetic F<strong>in</strong>d<strong>in</strong>gs <strong>in</strong> Genome-wide Analyses<br />

Susanne Lucae (MPI für Psychiatrie, München)<br />

E<strong>in</strong>leitung: Die Heritabilität <strong>der</strong> unipolaren Depression wird auf<br />

35 – 40 % geschätzt, allerd<strong>in</strong>gs blieb die Suche nach den ursächlich<br />

beteiligten Genen mit Hilfe von Kandidatengen-Analysen bisher<br />

weitgehend erfolglos. Seit wenigen Jahren s<strong>in</strong>d nun genomweite<br />

Analysen technisch möglich.<br />

Methode: Am Max-Planck-Institut für Psychiatrie führten wir e<strong>in</strong>e<br />

genomweite Assoziationsstudie zur unipolaren Depression mit<br />

zwei anschließenden Replikationsstudien durch. In funktionellen<br />

Analysen (mRNA-Expression, Mausmodell) konnte e<strong>in</strong> <strong>in</strong>teressantes<br />

Kandidatengen weiter untersucht und validiert werden.<br />

Diskussion / Ergebnisse: Es wurden bereits e<strong>in</strong>ige wenige genomweite<br />

Studien zur unipolaren Depression publiziert, an<strong>der</strong>e s<strong>in</strong>d <strong>in</strong><br />

Vorbereitung. Es wird die genomweite Analyse zur unipolaren Depression<br />

vorgestellt, die am Max-Planck-Institut für Psychiatrie<br />

durchgeführt wurde. Außerdem werden bereits publizierte genomweiten<br />

Studien zusammengefasst und diskutiert.<br />

002<br />

Corticosteroid Receptor Gene Variants and Experimental Stress<br />

Reactivity: Implications for the Development of Depressive Disor<strong>der</strong>s<br />

Stefan Wüst (ZI Mannheim, Genetische Epidemiologie)<br />

003<br />

Genetic F<strong>in</strong>d<strong>in</strong>gs <strong>in</strong> Personality as Risk Factors for Affective Disor<strong>der</strong>s<br />

Andreas Reif (Universität Würzburg, Psychiatrische Kl<strong>in</strong>ik)<br />

T. Nguyen, A. Strobel, C. Jacob, K.-P. Lesch<br />

Introduction: Neuroticism and related personality dimensions are<br />

etiologically heterogeneous traits with complex genetics. Def<strong>in</strong>ition<br />

of cl<strong>in</strong>ical phenotypes are not rooted <strong>in</strong> their neurobiology and respective<br />

animal models have consi<strong>der</strong>able limitations. Even more<br />

so, depression is a complex behavior with equally diverse un<strong>der</strong>ly<strong>in</strong>g<br />

neurobiological un<strong>der</strong>p<strong>in</strong>n<strong>in</strong>gs not readily expla<strong>in</strong>ed by simplistic<br />

models. Formal genetic studies however have consistently<br />

argued for the notion that high levels of Neuroticism as well as<br />

Cluster C personality disor<strong>der</strong>s are risk factors for later-life depression,<br />

especially <strong>in</strong> the presence of adverse life events.<br />

Discussion / Results: Although research on the neurobiology of<br />

those behaviors is still <strong>in</strong> its <strong>in</strong>fancy, several milestones have already<br />

been reached: Variation <strong>in</strong> gene expression were confirmed to play<br />

a predom<strong>in</strong>ant role <strong>in</strong> <strong>in</strong>dividual differences <strong>in</strong> complex traits <strong>in</strong>clud<strong>in</strong>g<br />

personality and behavior; gene x environment <strong>in</strong>teraction<br />

were established <strong>in</strong> humans and the nonhuman primate model;<br />

gene-phenotype correlations were substantiated by func tional neuroimag<strong>in</strong>g;<br />

as well as the notion that both genes and environmental<br />

factor impact on bra<strong>in</strong> development and thus set the stage for the<br />

susceptibility to depression is <strong>in</strong>creas<strong>in</strong>gly appreciated. Investigation<br />

of subtle alterations <strong>in</strong> the expression of genes of the serotonergic<br />

pathway, such as the seroton<strong>in</strong> transporter (5HTT), of correlations<br />

between 5HTT genotype and bra<strong>in</strong> activity, and of environmental<br />

variables <strong>in</strong>teract<strong>in</strong>g with 5HTT variants currently strengthen re-

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