Selected topics of the DGPPN Congress 2012

Abstract

This issue presents some selected topics from last year’s DGPPN Congress in November 2012, which might be of interest for the broad readership of our journal. Bridging the area of expertise between Neurology and Psychiatry, Hellmann-Regen et al. [1] deal with depressive syndromes representing a common feature in several neurological disorders. The most prominent example is the post-stroke depression on the one hand, while on the other hand, depression itself is a risk factor for developing cardiovascular diseases and ischemia. Depressive symptoms are also often related to other neurological conditions such as epilepsy, multiple sclerosis and Parkinson’s disease with impact on outcome and quality of life. Besides interesting findings of brain regions involved in the pathophysiology of this comorbidity, the authors also offer treatment recommendations. Deciphering the neuropathology of conversion of pre-clinical Alzheimer’s disease (AD) to clinical AD may lead to the development of new therapeutic strategies. Thal et al. [2] compared clinical AD, nondemented preclinical AD and non-AD control cases with respect to neuropathological alterations. They defined clinical AD to exhibit late stages of neurofibrillary tangles, amyloid and neuritic plaque pathology. In contrast, preclinical AD displays early stages of these lesions, but early neurofibrillary tangles, granulovascular degeneration and amyloid angiopathy without amyloid plaques can also be detected in non-AD controls, representing a pre-amyloid plaque stage. Additionally, the presence of soluble/dispersible As aggregates in the neuropil plays a role in the conversion of preclinical AD to full AD. The genetic background has an important influence on pathophysiological processes. In schizophrenia, heritability estimates amount from 60 to 80 %. Schwab and Wildenauer [3] update results from recent multistage genomewide association studies, according to which a set of 8300 independent SNPs contribute to a schizophrenia liability of 32 %. Several of these genes have meanwhile been confirmed, such as ZNF804A, TCF4 (encoding a transcription factor), the MHC region, CACNA1C (encoding calcium channel, voltage dependent, L-type, alpha 1C subunit) and ITIH3-ITIH4 (encoding inter-alpha globulin inhibitors H3 and H4). Same applies to ANK3 (encoding ankyrin 3) and the MIR137, encoding a microRNA which is a regulator of neuronal development. Further studies combining larger samples with deep sequencing technologies will extend our knowledge on the genetic background of psychiatric disorders. Also, gene–environmental interactions have been deemed an important factor in the pathophysiology of schizophrenia. Malchow et al. [4] investigated the impact of familial load and cannabis abuse on volumes of subcortical brain regions in first-episode patients. Patients with a family history of schizophrenia combined with previous cannabis abuse showed smaller volumes of the bilateral caudate nucleus compared to all other patients, implicating an interaction between the genetic background and cannabis abuse as environmental factor. The identified brain region plays an important role in the corticothalamic-cortical circuit, and dysfunction of the caudate nucleus may lead to disinhibition of the thalamus in schizophrenia. The neuropeptide oxytocin has been shown to be important for social cognition. Presenting direct versus averted gaze pictures to healthy probands, Montag et al. [5] A. Schmitt (&) P. Falkai Department of Psychiatry and Psychotherapy, Ludwig-Maximilians-University Munich, Nusbaumstr. 7, 80336 Munich, Germany e-mail: Andrea.Schmitt@med.uni-muenchen.de