@article{GerlachMaetzlerBroichetal.2011,
  author    = {Gerlach, Manfred and Maetzler, Walter and Broich, Karl and Hampel, Harald and Rems, Lucas and Reum, Torsten and Riederer, Peter and St{\"o}ffler, Albrecht and Streffer, Johannes and Berg, Daniela},
  title     = {Biomarker candidates of neurodegeneration in Parkinson's disease for the evaluation of disease-modifying therapeutics},
  series = {Journal of Neural Transmission},
  volume    = {119},
  journal   = {Journal of Neural Transmission},
  number    = {1},
  doi       = {10.1007/s00702-011-0682-x},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-133856},
  pages     = {39-52},
  year      = {2011},
  abstract  = {Reliable biomarkers that can be used for early diagnosis and tracking disease progression are the cornerstone of the development of disease-modifying treatments for Parkinson's disease (PD). The German Society of Experimental and Clinical Neurotherapeutics (GESENT) has convened a Working Group to review the current status of proposed biomarkers of neurodegeneration according to the following criteria and to develop a consensus statement on biomarker candidates for evaluation of disease-modifying therapeutics in PD. The criteria proposed are that the biomarker should be linked to fundamental features of PD neuropathology and mechanisms underlying neurodegeneration in PD, should be correlated to disease progression assessed by clinical rating scales, should monitor the actual disease status, should be pre-clinically validated, and confirmed by at least two independent studies conducted by qualified investigators with the results published in peer-reviewed journals. To date, available data have not yet revealed one reliable biomarker to detect early neurodegeneration in PD and to detect and monitor effects of drug candidates on the disease process, but some promising biomarker candidates, such as antibodies against neuromelanin, pathological forms of α-synuclein, DJ-1, and patterns of gene expression, metabolomic and protein profiling exist. Almost all of the biomarker candidates were not investigated in relation to effects of treatment, validated in experimental models of PD and confirmed in independent studies.},
  language  = {en}
}
@article{GellaSeguraDuranyetal.2011,
  author    = {Gella, Alejandro and Segura, M{\`o}nica and Durany, N{\´u}ria and Pfuhlmann, Bruno and St{\"o}ber, Gerald and Gawlik, Micha},
  title     = {Is Ankyrin a genetic risk factor for psychiatric phenotypes?},
  series = {BMC Psychiatry},
  volume    = {11},
  journal   = {BMC Psychiatry},
  number    = {103},
  doi       = {10.1186/1471-244X-11-103},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-137769},
  year      = {2011},
  abstract  = {Background Genome wide association studies reported two single nucleotide polymorphisms in ANK3 (rs9804190 and rs10994336) as independent genetic risk factors for bipolar disorder. Another SNP in ANK3 (rs10761482) was associated with schizophrenia in a large European sample. Within the debate on common susceptibility genes for schizophrenia and bipolar disorder, we tried to investigate common findings by analyzing association of ANK3 with schizophrenia, bipolar disorder and unipolar depression. Methods We genotyped three single nucleotide polymorphisms (SNPs) in ANK3 (rs9804190, rs10994336, and rs10761482) in a case-control sample of German descent including 920 patients with schizophrenia, 400 with bipolar affective disorder, 220 patients with unipolar depression according to ICD 10 and 480 healthy controls. Sample was further differentiated according to Leonhard's classification featuring disease entities with specific combination of bipolar and psychotic syndromes. Results We found no association of rs9804190 and rs10994336 with bipolar disorder, unipolar depression or schizophrenia. In contrast to previous findings rs10761482 was associated with bipolar disorder (p = 0.015) but not with schizophrenia or unipolar depression. We observed no association with disease entities according to Leonhard's classification. Conclusion Our results support a specific genetic contribution of ANK3 to bipolar disorder though we failed to replicate findings for schizophrenia. We cannot confirm ANK3 as a common risk factor for different diseases.},
  language  = {en}
}
@article{GellaSeguraDuranyetal.2011,
  author    = {Gella, Alejandro and Segura, Monica and Durany, Nuria and Pfuhlmann, Bruno and Stoeber, Gerald and Gawlik, Micha},
  title     = {Is Ankyrin a specific genetic risk factor for psychiatric phenotypes?},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-68732},
  year      = {2011},
  abstract  = {Background: Genome wide association studies reported two single nucleotide polymorphisms in ANK3 (rs9804190 and rs10994336) as independent genetic risk factors for bipolar disorder. Another SNP in ANK3 (rs10761482) was associated with schizophrenia in a large European sample. Within the debate on common susceptibility genes for schizophrenia and bipolar disorder, we tried to investigate common findings by analyzing association of ANK3 with schizophrenia, bipolar disorder and unipolar depression. Methods: We genotyped three single nucleotide polymorphisms (SNPs) in ANK3 (rs9804190, rs10994336, and rs10761482) in a case-control sample of German descent including 920 patients with schizophrenia, 400 with bipolar affective disorder, 220 patients with unipolar depression according to ICD 10 and 480 healthy controls. Sample was further differentiated according to Leonhard's classification featuring disease entities with specific combination of bipolar and psychotic syndromes. Results: We found no association of rs9804190 and rs10994336 with bipolar disorder, unipolar depression or schizophrenia. In contrast to previous findings rs10761482 was associated with bipolar disorder (p = 0.015) but not with schizophrenia or unipolar depression. We observed no association with disease entities according to Leonhard's classification. Conclusion: Our results support a specific genetic contribution of ANK3 to bipolar disorder though we failed to replicate findings for schizophrenia. We cannot confirm ANK3 as a common risk factor for different diseases.},
  subject      = {Schizophrenie},
  language  = {en}
}
@article{EgetemeirStennekenKoehleretal.2011,
  author    = {Egetemeir, Johanna and Stenneken, Prisca and Koehler, Saskia and Fallgatter, Andreas J. and Herrmann, Martin J.},
  title     = {Exploring the neural basis of real-life joint action: measuring brain activation during joint table setting with functional near-infrared spectroscopy},
  series = {FRONTIERS IN HUMAN NEUROSCIENCE},
  volume    = {5},
  journal   = {FRONTIERS IN HUMAN NEUROSCIENCE},
  number    = {9, Artikel 95},
  doi       = {10.3389/fnhum.2011.00095},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-137054},
  pages     = {1-9},
  year      = {2011},
  abstract  = {Many every-day life situations require two or more individuals to execute actions together. Assessing brain activation during naturalistic tasks to uncover relevant processes underlying such real-life joint action situations has remained a methodological challenge. In the present study, we introduce a novel joint action paradigm that enables the assessment of brain activation during real-life joint action tasks using functional near-infrared spectroscopy (fNIRS). We monitored brain activation of participants who coordinated complex actions with a partner sitting opposite them. Participants performed table setting tasks, either alone (solo action) or in cooperation with a partner (joint action), or they observed the partner performing the task (action observation). Comparing joint action and solo action revealed stronger activation (higher [oxy-Hb]-concentration) during joint action in a number of areas. Among these were areas in the inferior parietal lobule (IPL) that additionally showed an overlap of activation during action observation and solo action. Areas with such a close link between action observation and action execution have been associated with action simulation processes. The magnitude of activation in these IPL areas also varied according to joint action type and its respective demand on action simulation. The results validate fNIRS as an imaging technique for exploring the functional correlates of interindividual action coordination in real-life settings and suggest that coordinating actions in real-life situations requires simulating the actions of the partner.},
  language  = {en}
}
@article{BonnSchmittAsan2011,
  author    = {Bonn, Maria and Schmitt, Angelika and Asan, Esther},
  title     = {Double and triple in situ hybridization for coexpression studies: combined fluorescent and chromogenic detection of neuropeptide Y (NPY) and serotonin receptor subtype mRNAs expressed at different abundance levels},
  series = {Histochemistry and Cell Biology},
  volume    = {137},
  journal   = {Histochemistry and Cell Biology},
  number    = {1},
  doi       = {10.1007/s00418-011-0882-3},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-135229},
  pages     = {Nov 24},
  year      = {2011},
  abstract  = {Multiple fluorescence in situ hybridization is the method of choice for studies aimed at determining simultaneous production of signal transduction molecules and neuromodulators in neurons. In our analyses of the monoamine receptor mRNA expression of peptidergic neurons in the rat telencephalon, double tyramide-signal-amplified fluorescence in situ hybridization delivered satisfactory results for coexpression analysis of neuropeptide Y (NPY) and serotonin receptor 2C (5-HT2C) mRNA, a receptor subtype expressed at high-to-moderate abundance in the regions analyzed. However, expression of 5-HT1A mRNA, which is expressed at comparatively low abundance in many telencephalic areas, could not be unequivocally identified in NPY mRNA-reactive neurons due to high background and poor signal-to-noise ratio in fluorescent receptor mRNA detections. Parallel chromogenic in situ hybridization provided clear labeling for 5-HT1A mRNA and additionally offered the possibility to monitor the chromogen deposition at regular time intervals to determine the optimal signal-to-noise ratio. We first developed a double labeling protocol combining fluorescence and chromogenic in situ hybridization and subsequently expanded this variation to combine double fluorescence and chromogenic in situ hybridization for triple labelings. With this method, we documented expression of 5-HT2C and/or 5-HT1A in subpopulations of telencephalic NPY-producing neurons. The method developed in the present study appears suitable for conventional light and fluorescence microscopy, combines advantages of fluorescence and chromogenic in situ hybridization protocols and thus provides a reliable non-radioactive alternative to previously published multiple labeling methods for coexpression analyses in which one mRNA species requires highly sensitive detection.},
  language  = {en}
}
@article{BiehlDreslerReifetal.2011,
  author    = {Biehl, Stefanie C. and Dresler, Thomas and Reif, Andreas and Scheuerpflug, Peter and Deckert, J{\"u}rgen and Herrmann, Martin J.},
  title     = {Dopamine Transporter (DAT1) and Dopamine Receptor D4 (DRD4) Genotypes Differentially Impact on Electrophysiological Correlates of Error Processing},
  series = {PLoS One},
  volume    = {6},
  journal   = {PLoS One},
  number    = {12},
  doi       = {10.1371/journal.pone.0028396},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-137930},
  pages     = {e28396},
  year      = {2011},
  abstract  = {Recent studies as well as theoretical models of error processing assign fundamental importance to the brain's dopaminergic system. Research about how the electrophysiological correlates of error processing—the error-related negativity (ERN) and the error positivity (Pe)—are influenced by variations of common dopaminergic genes, however, is still relatively scarce. In the present study, we therefore investigated whether polymorphisms in the DAT1 gene and in the DRD4 gene, respectively, lead to interindividual differences in these error processing correlates. One hundred sixty participants completed a version of the Eriksen Flanker Task while a 26-channel EEG was recorded. The task was slightly modified in order to increase error rates. During data analysis, participants were split into two groups depending on their DAT1 and their DRD4 genotypes, respectively. ERN and Pe amplitudes after correct responses and after errors as well as difference amplitudes between errors and correct responses were analyzed. We found a differential effect of DAT1 genotype on the Pe difference amplitude but not on the ERN difference amplitude, while the reverse was true for DRD4 genotype. These findings are in line with predictions from theoretical models of dopaminergic transmission in the brain. They furthermore tie results from clinical investigations of disorders impacting on the dopamine system to genetic variations known to be at-risk genotypes.},
  language  = {en}
}
@article{BartlScholzHinterbergeretal.2011,
  author    = {Bartl, Jasmin and Scholz, Claus-J{\"u}rgen and Hinterberger, Margareta and Jungwirth, Susanne and Wichart, Ildiko and Rainer, Michael K. and Kneitz, Susanne and Danielczyk, Walter and Tragl, Karl H. and Fischer, Peter and Riederer, Peter and Gr{\"u}nblatt, Edna},
  title     = {Disorder-specific effects of polymorphisms at opposing ends of the Insulin Degrading Enzymegene},
  series = {BMC Medical Genetics},
  volume    = {12},
  journal   = {BMC Medical Genetics},
  number    = {151},
  doi       = {10.1186/1471-2350-12-15},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-137744},
  year      = {2011},
  abstract  = {Background Insulin-degrading enzyme (IDE) is the ubiquitously expressed enzyme responsible for insulin and amyloid beta (Aβ) degradation. IDE gene is located on chromosome region 10q23-q25 and exhibits a well-replicated peak of linkage with Type 2 diabetes mellitus (T2DM). Several genetic association studies examined IDE gene as a susceptibility gene for Alzheimer's disease (AD), however with controversial results. Methods We examined associations of three IDE polymorphisms (IDE2, rs4646953; IDE7, rs2251101 and IDE9, rs1887922) with AD, Aβ42 plasma level and T2DM risk in the longitudinal Vienna Transdanube Aging (VITA) study cohort. Results The upstream polymorphism IDE2 was found to influence AD risk and to trigger the Aβ42 plasma level, whereas the downstream polymorphism IDE7 modified the T2DM risk; no associations were found for the intronic variant IDE9. Conclusions Based on our SNP and haplotype results, we delineate the model that IDE promoter and 3' untranslated region/downstream variation may have different effects on IDE expression, presumably a relevant endophenotype with disorder-specific effects on AD and T2DM susceptibility.},
  language  = {en}
}