@article{Canli2007, abstract = {The gene encoding the serotonin transporter (5-HTT) contains a regulatory variation that has been associated with anxiety-related traits and susceptibility for depression. Here we highlight recent discoveries related to allelic variation of 5-HTT function with respect to emotion regulation and social behavior, drawing from an interdisciplinary perspective of behavioral genetics and cognitive neuroscience. Following a reductionistic path that leads from gene-behavior association studies to neuroimaging and epigenetic studies, we compare two models of 5-HTT-dependent modulation of brain activity and discuss the role of life stress experience in modifying 5-HTT function in the brain. Integration of these findings suggests that the impact of the 5-HTT gene on behavior is much broader than is commonly appreciated and may have a role in social cognition.}, author = {Canli, Turhan and Lesch, Klaus-Peter}, doi = {10.1038/nn1964}, journal = {Nature Neuroscience}, month = {aug}, pages = {1103-1109}, title = {Long Story Short: The Serotonin Transporter in Emotion Regulation and Social Cognition}, url = {http://www.nature.com/articles/nn1964.pdf}, volume = {10}, year = {2007} } @article{Congdon2007, abstract = {Impulsivity, a highly prevalent symptom in multiple psychiatric disorders, is a partially heritable trait influenced by specific biological mechanisms. In particular, dopamine is proposed to play a role in impulsive behaviors and recent studies have implicated functional polymorphisms of dopamine-related genes in impulsive behaviors across different clinical and behavioral classifications. However, most have not isolated the impulsivity construct per se as a biologically based and measurable endophenotype. The present study was therefore undertaken in a sample of healthy adults to investigate the influence of two candidate dopaminergic gene polymorphisms (DRD4 and DAT) on the endophenotype of impulsivity, which we operationalized as behavioral inhibition during the Stop-signal task. We recruited an ethnically diverse sample of 119 healthy adults to complete a self-report questionnaire of impulsivity and to perform a Stop-signal task. We report significant differences in inhibitory control between individuals with at least one 7-repeat allele of the DRD4 polymorphism, as well as an interaction between DRD4 and DAT genotypes, on inhibitory control. Results of the present study support the influence of dopaminergic variation on impulsive-related measures, as well as the advantage of using measures which are likely more sensitive to the effects of such genetic variation.}, author = {Congdon, Eliza and Lesch, Klaus Peter and Canli, Turhan}, doi = {10.1002/ajmg.b.30557}, journal = {American Journal of Medical Genetics Part B: Neuropsychiatric Genetics}, month = {may}, pages = {27-32}, title = {Analysis of DRD4 and DAT Polymorphisms and Behavioral Inhibition in Healthy Adults: Implications for Impulsivity}, url = {https://www.researchgate.net/profile/Turhan_Canli/publication/6306885_Analysis_of_DRD4_and_DAT_Polymorphisms_and_Behavioral_Inhibition_in_Healthy_Adults_Implications_for_Impulsivity/links/0fcfd51101a4339b2e000000.pdf}, volume = {147B}, year = {2007} } @article{Fox2007, author = {Fox, Meredith A. and Andrews, Anne M. and Wendland, Jens R. and Lesch, Klaus-Peter and Holmes, Andrew and Murphy, Dennis L.}, doi = {10.1007/s00213-007-0910-0}, journal = {Psychopharmacology}, month = {aug}, pages = {147-166}, title = {A pharmacological analysis of mice with a targeted disruption of the serotonin transporter}, url = {https://www.researchgate.net/profile/Anne_Andrews/publication/6126502_A_pharmacological_analysis_of_mice_with_a_targeted_disruption_of_the_serotonin_transporter/links/02bfe510b1964b46ae000000.pdf}, volume = {195}, year = {2007} } @article{Fritzen2007, abstract = {Investigations regarding the regulation of adult neurogenesis, i.e., the generation of new neurons from progenitor cells, have revealed a high degree of complexity. Although the pleiotropic messenger molecule nitric oxide (NO) has been suggested to modulate adult neurogenesis, the evidence is inconclusive due to the presence of different NO synthase isoforms in the brain. We therefore investigated whether stem cell proliferation or survival is altered in mice lacking neuronal nitric oxide synthase (NOS-I) or both endothelial and neuronal NOS (NOS-I/-III double knockout). While proliferation of neural stem cells was only numerically, but not significantly increased in NOS-I knockdown animals, the survival of newly formed neurons was substantially higher in NOS-I-deficient mice. In contrast, NOS-I/-III double knockout had significantly decreased survival rates. QRT-PCR in NOS-I-deficient mice revealed neither NOS-III upregulation compensating for the loss of NOS-I, nor alterations in VEGF levels as found in NOS-III-deficient animals. As changes in BDNF expression or protein levels were observed in the cortex, cerebellum and striatum, but not the hippocampus, the increase in stem cell survival appears not to be due to a BDNF mediated mechanism. Finally, NOS-I containing neurons in the dentate gyrus are rare and not localized close to progenitor cells, rendering direct NO effects on these cells unlikely. In conclusion, we suggest that NO predominantly inhibits the survival of new-born cells, by an indirect mechanism not involving BDNF or VEGF. Together, these results emphasize the important role of the different NOS isoforms with respect to adult neurogenesis.}, author = {Fritzen, Sabrina and Schmitt, Angelika and Köth, Katharina and Sommer, Claudia and Lesch, Klaus-Peter and Reif, Andreas}, doi = {10.1016/j.mcn.2007.02.021}, journal = {Molecular and Cellular Neuroscience}, month = {jul}, pages = {261-271}, title = {Neuronal nitric oxide synthase (NOS-I) knockout increases the survival rate of neural cells in the hippocampus independently of BDNF}, url = {https://www.researchgate.net/profile/Angelika_Schmitt/publication/6368940_Neuronal_nitric_oxide_synthase_NOS-I_knockout_increases_the_survival_rate_of_neural_cells_in_the_hippocampus_independently_of_BDNF/links/0912f51372df69574c000000.pdf}, volume = {35}, year = {2007} } @article{Gutknecht2007, abstract = {Variation in the tryptophan hydroxylase-2 gene (TPH2) coding for the rate-limiting enzyme of serotonin (5-HT) synthesis in the brain modulates responses of limbic circuits to emotional stimuli and has been linked to a spectrum of clinical populations characterized by emotional dysregulation. Here, we tested a set of common single nucleotide polymorphisms (SNPs) in and downstream of the transcriptional control region of TPH2 for association with personality traits and with risk for personality disorders in two cohorts comprising of 336 healthy individuals and 420 patients with personality disorders. Personality dimensions were assessed by the Tridimensional Personality Questionnaire (TPQ) and the revised NEO Personality Inventory (NEO-PI-R). Personality disorders were diagnosed with the Structured Clinical Interview of DSM-IV and were allocated to clusters A, B, and C. Individual SNP and haplotype analyses revealed significant differences in genotype frequencies between controls and cluster B as well as cluster C patients, respectively. In both patient groups, we observed overrepresentation of T allele carriers of a functional polymorphism in the upstream regulatory region of TPH2 (SNP G-703T, rs4570625) which was previously shown to bias responsiveness of the amygdala, a structure critically involved in emotionality. Furthermore, significant effects of TPH2 variants on anxiety-related traits defined primarily by the TPQ Harm Avoidance were found in healthy individuals. The results link potentially functional TPH2 variants to personality traits related to emotional instability as well as to cluster B and cluster C personality disorders. These findings implicate alterations of 5-HT synthesis in emotion regulation and confirm TPH2 as a susceptibility and/or modifier gene of affective spectrum disorders.}, author = {Gutknecht, Lise and Jacob, Christian and Strobel, Alexander and Kriegebaum, Claudia and Müller, Johannes and Zeng, Yong and Markert, Christoph and Escher, Andrea and Wendland, Jens and Reif, Andreas and Mössner, Rainald and Gross, Cornelius and Brocke, Burkhard and Lesch, Klaus-Peter}, doi = {10.1017/s1461145706007437}, month = {jul}, title = {Tryptophan hydroxylase-2 gene variation influences personality traits and disorders related to emotional dysregulation}, url = {https://academic.oup.com/ijnp/article-pdf/10/3/309/2683596/10-3-309.pdf}, year = {2007} } @article{Herrmann2007, abstract = {Prior studies reported that functional variants of both the serotonin transporter (5-HTT) and tryptophan hydroxylase-2 genes (TPH2), 2 key regulators of the serotonergic signaling pathway, modulate amygdala activation during emotional processing. We addressed the question whether these 2 gene variants modulate each other, using an emotional picture-processing task. Specifically, we measured event-related potentials (ERPs) during a passive emotional picture perception task, focusing on ERPs for the early posterior negativity (EPN) around 240 ms and for the slow wave starting at 315 ms. We found evidence for increased neural activity at 240 ms in individuals who carried 1 or 2 copies of the low-expression short variant of the 5-HTT. Carriers of T variant of the TPH2 also showed a tendency toward increased neural activity at 240 ms. Moreover, we observed an additive effect of both genotypes for EPN, with highest neural activity to emotional stimuli in individuals carrying combination of both short variant of 5-HTT and T variant of TPH2. Our results indicate that both the 5-HTT and the TPH2 genotypes modulate the sensory encoding of affective stimuli during early steps of visual processing and reveal additive effects of 2 genes in the serotonergic control of emotion regulation.}, author = {Herrmann, Martin J. and Huter, Theresa and Müller, Frauke and Mühlberger, Andreas and Pauli, Paul and Reif, Andreas and Renner, Tobias and Canli, Turhan and Fallgatter, Andreas J. and Lesch, Klaus-Peter}, doi = {10.1093/cercor/bhl026}, journal = {Cerebral Cortex}, month = {jun}, pages = {1160-1163}, title = {Additive Effects of Serotonin Transporter and Tryptophan Hydroxylase-2 Gene Variation on Emotional Processing}, url = {https://academic.oup.com/cercor/article-pdf/17/5/1160/984895/bhl026.pdf}, volume = {17}, year = {2007} } @article{Hünnerkopf2007, abstract = {The involvement in neural plasticity and the mediation of effects of repeated stress exposure and long-term antidepressant treatment on hippocampal neurogenesis supports a critical role of brain-derived neurotrophic factor (BDNF) in the pathophysiology of affective and other stress-related disorders. A previously reported valine to methionine substitution at amino-acid position 66 (BDNF Val66Met) seems to account for memory disturbance and hippocampal dysfunction. In the present study, we evaluated the impact of the BDNF Val66Met polymorphism on individual differences in personality traits in a sample of healthy volunteers in relation to other common gene variants thought to be involved in the pathophysiology of affective disorders, such as the serotonin transporter promoter polymorphism (5-HTTLPR) and a variable number of tandem repeat polymorphism of the dopamine transporter gene (DAT VNTR). Personality traits were assessed using the NEO personality inventory (NEO-PI-R) and Tridimensional Personality Questionnaire (TPQ). There was a significant DAT VNTR-dependent association between NEO-PI-R Neuroticism and the BDNF Val66Met polymorphism. Among individuals with at least one copy of the DAT 9-repeat allele, carriers of the BDNF Met allele exhibited significantly lower Neuroticism scores than noncarriers. This interaction was also observed for TPQ Harm Avoidance, a personality dimension related to Neuroticism. Our results support the notion that allelic variation at the BDNF locus--in interaction with other gene variants--influences anxiety- and depression-related personality traits.}, author = {Hünnerkopf, Regina and Strobel, Alexander and Gutknecht, Lise and Brocke, Burkhard and Lesch, Klaus Peter}, doi = {10.1038/sj.npp.1301383}, journal = {Neuropsychopharmacology}, month = {mar}, pages = {2552-2560}, title = {Interaction between BDNF Val66Met and Dopamine Transporter Gene Variation Influences Anxiety-Related Traits}, url = {https://www.nature.com/articles/1301383.pdf}, volume = {32}, year = {2007} } @article{Jacob2007, author = {Jacob, Christian P. and Romanos, Jasmin and Dempfle, Astrid and Heine, Monika and Windemuth-Kieselbach, Christine and Kruse, Anja and Reif, Andreas and Walitza, Susanne and Romanos, Marcel and Strobel, Alexander and Brocke, Burkhard and Schäfer, Helmut and Schmidtke, Armin and Böning, Jobst and Lesch, Klaus-Peter}, doi = {10.1007/s00406-007-0722-6}, journal = {European Archives of Psychiatry and Clinical Neuroscience}, month = {apr}, pages = {309-317}, title = {Co-morbidity of adult attention-deficit/hyperactivity disorder with focus on personality traits and related disorders in a tertiary referral center}, url = {https://www.researchgate.net/profile/Alexander_Strobel/publication/51383417_Co-morbidity_of_adult_attention-deficithyperactivity_disorder_with_focus_on_personality_traits_and_related_disorders_in_a_tertiary_referral_center/links/02e7e52120c4413464000000.pdf}, volume = {257}, year = {2007} } @article{Kraus2007, author = {Kraus, Michael R. and Al-Taie, Oliver and Schäfer, Arne and Pfersdorff, Matthias and Lesch, Klaus–Peter and Scheurlen, Michael}, doi = {10.1053/j.gastro.2007.02.053}, journal = {Gastroenterology}, month = {apr}, pages = {1279-1286}, title = {Serotonin-1A Receptor Gene HTR1A Variation Predicts Interferon-Induced Depression in Chronic Hepatitis C}, url = {https://oadoi.org/10.1053/j.gastro.2007.02.053}, volume = {132}, year = {2007} } @article{Lesch2007, author = {Lesch, Klaus-Peter}, doi = {10.1038/sj.embor.7401008}, journal = {EMBO Reports}, month = {jul}, title = {Linking emotion to the social brain: The role of the serotonin transporter in human social behaviour}, url = {http://embor.embopress.org/content/embor/8/1S/S24.full.pdf}, volume = {8}, year = {2007} } @article{Mössner2007, abstract = { The 5-HT3 receptor is unique among the serotonin receptors in that it is a ligand-gated ion channel. Dysfunction of the serotonin system is thought to contribute to the pathogenesis of obsessive—compulsive disorder (OCD). Apart from the standard treatment with serotonin reuptake inhibitors and behavioural therapy, a 5-HT3 receptor antagonist has recently been shown to benefit some OCD patients, suggesting the 5-HT3 receptor as a serotonergic candidate gene in the polygenic aetiology of OCD. A functional regulatory variant of the 5-HT3A receptor influences 5-HT 3 receptor expression, serotonin metabolites in cerebrospinal fluid, and amygdala reactivity. We therefore assessed whether this C178T variant influences the risk of developing OCD. In a family-based approach employing the transmission disequilibrium test, we analysed a unique sample of 75 children and adolescents with OCD, as well as their biological parents. We found no evidence for a preferential transmission of either allele to the patients — the estimated transmission rate for the C allele was 0.51 (95% CI 0.36—0.65). This argues against an involvement of the 5-HT3A receptor in the polygenic aetiology of early-onset OCD. }, author = {Mössner, Rainald and Döring, Nicole and Scherag, André and Schafer, H. and Schäfer, Helmut and Herpertz-Dahlmann, Beate and Remschmidt, Helmut and Schulz, Eberhard and Renner, Tobias and Wewetzer, Christoph and Warnke, Andreas and Lesch, Klaus-Peter and Walitza, Susanne}, doi = {10.1177/0269881106073560}, journal = {Journal of Psychopharmacology}, month = {dec}, pages = {833-836}, title = {Transmission disequilibrium analysis of the functional 5-HT3A receptor variant C178T in early-onset obsessive compulsive disorder}, url = {https://www.researchgate.net/profile/Andre_Scherag2/publication/6545338_Transmission_disequilibrium_analysis_of_the_functional_5-HT3A_receptor_variant_C178T_in_early-onset_obsessive_compulsive_disorder/links/02bfe5113531285e23000000.pdf}, volume = {21}, year = {2007} } @article{Müller2007, abstract = {Positive affect and the activity of the neurotransmitter dopamine seem to shift the balance between cognitive flexibility vs stability towards increased flexibility. Here we examined the impact of prospective monetary gains on this balance. Seventy healthy volunteers performed a set-shifting task comprising a condition in which a bias towards new stimuli helped to overcome perseveration and increased flexibility, and a second condition in which directing attention towards new stimuli increased distractibility. From previous studies of executive functions, two contrasting predictions can be derived: the prospect of monetary gains might either increase cognitive flexibility due to a dopamine release in the prefrontal cortex or increase stability due to an assessment of high utility of action processed in the anterior cingulated cortex and orbitofrontal cortex. Overall, we observed increased cognitive stability in the face of prospective gains (η² = 7%). However, this effect was modulated by the subjective evaluation of the reward cues: participants who reported increasing their effort in response to reward cues showed increased cognitive stability, whereas those who reported a positive and relaxed attitude towards the reward cues showed increased flexibility (η² = 11%). The results thus suggest that the flexibility–stability balance is modulated by the perceived effort needed to receive the potential reward. On a neuropsychological level, an interaction of dopaminergic and noradrenergic processes might be involved in the allocation of control.}, author = {Müller, Johannes and Dreisbach, Gesine and Goschke, Thomas and Hensch, Tilman and Lesch, Klaus-Peter and Brocke, Burkhard}, doi = {10.1111/j.1460-9568.2007.05949.x}, journal = {European Journal of Neuroscience}, month = {jan}, pages = {3661-3668}, title = {Dopamine and cognitive control: The prospect of monetary gains influences the balance between flexibility and stability in a set-shifting paradigm}, url = {https://oadoi.org/10.1111/j.1460-9568.2007.05949.x}, volume = {26}, year = {2007} } @article{Numachi2007, abstract = {We examined the hyperthermic and lethal toxic effects of methamphetamine in dopamine transporter (DAT) and/or serotonin transporter (SERT) knockout (KO) mice. Methamphetamine (45 mg/kg) caused significant hyperthermia even in the mice with a single DAT gene copy and no SERT copies (DAT+/- SERT-/- mice). Mice with no DAT copies and a single SERT gene copy (DAT-/- SERT+/- mice) showed significant but reduced hyperthermia when compared to wild-type mice after methamphetamine. Surprisingly, DAT/SERT double KO mice exhibited a paradoxical hypothermia after methamphetamine. These results demonstrate that methamphetamine exerts a hyperthermic effect via DAT, or via SERT, in the absence of DAT. The selective norepinephrine transporter blocker (20 mg/kg nisoxetine) caused hyperthermia in DAT/SERT double KO mice, suggesting that the norepinephrine system is not responsible for methamphetamine-induced paradoxical hypothermia in the double KO mice. DAT gene deletion in mice strikingly increased LD50 of methamphetamine by 1.7-1.8 times that of wild-type mice, suggesting that the lethal toxic effect of methamphetamine is mainly dependent on DAT. Moreover, dissociation between hyperthermic and lethal toxic effects of methamphetamine in DAT single KO mice and DAT/SERT double KO mice suggest that hyperthermia is not a prerequisite for methamphetamine-induced lethality. Methamphetamine (45 mg/kg) significantly increased mRNA of interleukin-1beta, which is the major endogenous pyrogen, in the hypothalamus of wild-type mice but not in DAT/SERT double KO mice, which provides a partial mechanism of methamphetamine-induced paradoxical hypothermia. These results suggest that DAT and SERT are key molecules for hyperthermic and lethal toxic effects of methamphetamine.}, author = {Numachi, Yohtaro and Ohara, Arihisa and Yamashita, Motoyasu and Fukushima, Setsu and Kobayashi, Hideaki and Hata, Harumi and Watanabe, Hidekazu and Hall, Frank Scott and Lesch, Klaus-Peter and Murphy, Dennis L. and Uhl, George R. and Sora, Ichiro}, doi = {10.1016/j.ejphar.2007.06.022}, journal = {European Journal of Pharmacology}, month = {oct}, pages = {120-128}, title = {Methamphetamine-induced hyperthermia and lethal toxicity: Role of the dopamine and serotonin transporters}, url = {https://www.researchgate.net/profile/Hideaki_Kobayashi/publication/6166493_Methamphetamine-induced_hyperthermia_and_lethal_toxicity_Role_of_the_dopamine_and_serotonin_transporters/links/0fcfd512bfe5e5c307000000.pdf}, volume = {572}, year = {2007} } @article{Reif2007, abstract = {Aggressive behavior is influenced by variation in genes of the serotonergic circuitry and early-life experience alike. The present study aimed at investigating the contribution of polymorphisms shown to moderate transcription of two genes involved in serotonergic neurotransmission (serotonin transporter, 5HTT, and monoamine oxidase A, MAOA) to the development of violence and to test for gene-environment interactions relating to adverse childhood environment. A cohort of 184 adult male volunteers referred for forensic assessment participated in the study. Each individual was assigned to either a violent or a nonviolent group. Logistic regression was performed and the best-fitting model, with a predictive power of 74%, revealed independent effects of adverse childhood environment and MAOA genotype. High environmental adversity during childhood was associated significantly with violent behavior. Forty-five percent of violent, but only 30% of nonviolent individuals carried the low-activity, short MAOA allele. Most interestingly, an interaction effect between childhood environment and 5HTT genotype on violent behavior was found in that high adversity during childhood impacted only the later-life violence if the short promoter alleles were present. These findings indicate complex interactions between genetic variation of the serotonergic circuitry and environmental factors arguing against simplistic, mono-causal explanations of violent behavior.}, author = {Reif, Andreas and Rösler, Michael and Freitag, Christine M. and Schneider, Marc and Eujen, Andrea and Kissling, Christian and Wenzler, Denise and Jacob, Christian P. and Retz-Junginger, Petra and Thome, Johannes and Lesch, Klaus-Peter and Retz, Wolfgang}, doi = {10.1038/sj.npp.1301359}, journal = {Neuropsychopharmacology}, month = {mar}, pages = {2375-2383}, title = {Nature and Nurture Predispose to Violent Behavior: Serotonergic Genes and Adverse Childhood Environment}, url = {http://www.nature.com/articles/1301359.pdf}, volume = {32}, year = {2007} } @article{Reif2007_2, abstract = {Forty years after the initial discovery of neurogenesis in the postnatal brain of the rat, convincing evidence has been accrued that functional neurons are generated throughout the entire lifespan, particularly in the dentate gyrus (DG) and the subventricular zone (SVZ). This phenomenon has been termed adult neurogenesis (AN) and while it was detected in all examined mammalian species including humans, the physiological role of this process remains unknown. Although a plethora of animal studies indicate an involvement of AN in the pathophysiology of depression, this view has recently kindled considerable controversy. Pertinent studies in humans failed to confirm a role of reduced hippocampal neural stem cell proliferation (NSP) in depression but suggest a contribution to the pathophysiology of schizophrenia. The functional relevance of disturbed AN may encompass erroneous temporal encoding of new memory traces, thereby contributing to cognitive deficits observed in schizophrenia. This AN-hypothesis of schizophrenia is supported by neuroimaging, as well as by several genetically modified rodent models, e.g. reelin and NPAS3 knockout mice. Furthermore, several genes impacting on AN, including NPAS3, were also found to be associated with schizophrenia by case-control studies. In conclusion, several lines of evidence suggest that reduced AN may contribute to the etiopathogenesis of schizophrenic disorders, whereas it does not seem to be a critical risk factor for affective disorders.}, author = {Reif, Andreas and Schmitt, Angelika and Fritzen, Sabrina and Lesch, Klaus-Peter}, doi = {10.1007/s00406-007-0733-3}, journal = {European Archives of Psychiatry and Clinical Neuroscience}, month = {sep}, pages = {290-299}, title = {Neurogenesis and schizophrenia: dividing neurons in a divided mind? Eur Arch Psychiatry Clin Neurosci}, url = {https://link.springer.com/content/pdf/10.1007/s00406-007-0733-3.pdf}, volume = {257}, year = {2007} } @incollection{Scharnagl2007, author = {Scharnagl, Hubert and Zouboulis, Christos C. and Willenberg, Holger S. and Yazdanbakhsh, Karina and Wenning, Matthias and Şenaylı, Atilla and Zietz, Christian and Wesselborg, Sebastian and Zarins, Christopher K. and Zhao, Yun and Zeldin, Darryl C. and Yao, Zhirong and Wessels, Andy and Zimmermann, Marc and März, Winfried and Böhm, Markus and Luger, Thomas A. and Fracassi, Federico and Diana, Alessia and Frieling, Thomas and Mac, Susanna and Ariceta, Gema and Donoghue, Dan and Batlle, Daniel and Kohl, Susanne and Syed, Ehteshamudin and Sznajder, Jacob I. and Pfister, Markus and Kamat, Deepak and Leung, Alexander K. C. and Schwarz, Thomas and Frank, Jorge and Schinner, Sven and Bornstein, Stefan R. and Schiller, Meinhard and Nashan, Dorothée and Sunderkötter, Cord and Berneburg, Mark and Laing, Nigel G. and Beggs, Alan H. and Goebel, Hans H. and Loots, Du Toit and Sahota, Amrik and Tischfield, Jay A. and Simmonds, H. Anne and Dietmaier, Wolfgang and Hartmann, Arndt and Hershfield, Michael S. and Suneja, Manish and Schuchmann, Edward H. and Berghe, Georges and Thomas, Christie P. and Jaeken, Jaak and Powers, James M. and Bonkovsky, Herbert L. and Thapar, Manish and Mathur, Sishir and Denson, Lee A. and Kuilenburg, André B. P. and Gennip, Albert H. and Hul, Wim and Vanhoenacker, Filip and Frasch, Karel and Jäger, Markus and Mohebbi, Nilufar and Wagner, Carsten A. and Lindstedt, Malin and Borrebaeck, Carl and Bezdekova, Michala and Brychtova, Svetlana and Kolar, Zdenek and Brychta, Tomas and Kucerova, Renata and Bienova, Martina and Fischer, Tobias W. and Paus, Ralf and Haack, Birgit and Kins, Stefan and Beyreuther, Konrad and Ertürk, Sehsuvar and Kutlay, Sim and Emberger, Michael and Hintner, Helmut and McGovern, Margaret and Hawranek, Thomas and Danzeisen, Ruth and Ludolph, Albert C. and Estrella, Michelle M. and Atta, Mohamed G. and Thangaraj, Kumarasamy and Rajender, Singh and Schnog, John-B. and Gerdes, Victor E. A. and Ma, Patrick T. S. and Scaradavou, Andromachi and Gattermann, Norbert and Ma, Michael L. H. and Baumer, Alessandra and Schillinger, Wolfgang and Hasenfuss, Gerd and Bas, Murat and Kojda, Georg and Brehler, Randolf and Sezer, Engin and Stürzl, Michael and Klein, Peter and Mumm, Steven and Adler, Guido and Kiezebrink, Kirsty and Knutsen, Alan P. and Larsson, Henrik and Viding, Essi and Cate, Hugo Ten and Stoller, James K. and Lomas, David A. and Eser, Daniela and Rupprecht, Rainer and Simonaro, Calogera M. and Siepe, Matthias and Beyersdorf, Friedhelm and Liebe, Volker and Kaden, Jens J. and Bekeredjian, Raffi and Frey, Norbert and Fencl, Pavel and Ma, Lucia K. and Ibrahimi, Omar A. and Mohammadi, Moosa and Hoffmann, Michael M. and Stork, Björn and Stöckler-Ipsiroglu, Sylvia and Fischer, Avi and Mehta, Davendra and Seiler, Jens and Rotter, Martin and Leaf, Alexander and Sen-Chowdhry, Srijita and Ward, Deirdre and McKenna, William J. and Mogensen, Jens and Manfredi, Roberto and Sebes, Jeno and Ginès, Pere and Guevara, Mónica and Johnson, Colin A. and Wasserstein, Melissa P. and Melles∗, Damian C. and Marie, S. and Buckley, Mark G. and Dent, Gordon and Holgate, Stephen T. and Klockgether, Thomas and Kohlschütter, Alfried and Summerhill, Eleanor M. and McCool, F. Dennis and McGill, Rita L. and Endo, Mayumi and Paoletti, Rodolfo and Cignarella, Andrea and Digilio, M. Cristina and Marino, Bruno and Sarkozy, Anna and Dallapiccola, Bruno and Roberts-Thomson, Kurt C. and Kalman, Jonathan M. and McQuinn, Tim and Ma, Siobhan D. and Burri, Haran and Pozza, Robert Dalla and Lesch, Klaus-Peter and Bourgeron, Thomas and Kanaan, Nada and Berg, Bruno and Desnick, Robert J. and Goffin, Eric}, doi = {10.1007/978-0-387-70909-3_17}, journal = {Encyclopedia of Molecular Mechanisms of Disease}, month = {jan}, pages = {12-12}, title = {Acid Sphingomyelinase-Deficient Niemann–Pick Disease}, url = {https://oadoi.org/10.1007/978-0-387-70909-3_17}, year = {2007} } @article{Schmitt2008, author = {Schmitt, Angelika G. and Hall, F. Scott and Perona, Maria T. G. and Ortega, Gabriela and Hofmann, Miryame and Gagel, Carola and Sora, I. and Uhl, G. R. and Riederer, Peter and Lesch, Klaus-Peter and Gerlach, Manfred and Gruenblatt, Edna}, month = {jan}, title = {Methylphenidate treatment and stress differentially modify gene expression of immediate early genes in the DAT knockout mouse, a mouse model for ADHD}, year = {2008} } @article{Selch2007, author = {Selch, Sandra and Strobel, Alexander and Haderlein, Julia and Meyer, Jobst and Jacob, Christian P. and Schmitt, Angelika and Lesch, Klaus-Peter and Reif, Andreas}, doi = {10.1016/j.biopsych.2006.08.030}, journal = {Biological Psychiatry}, month = {may}, pages = {1211-1214}, title = {MLC1 Polymorphisms Are Specifically Associated with Periodic Catatonia, a Subgroup of Chronic Schizophrenia}, url = {https://www.researchgate.net/profile/Angelika_Schmitt/publication/6591458_MLC1_Polymorphisms_Are_Specifically_Associated_with_Periodic_Catatonia_a_Subgroup_of_Chronic_Schizophrenia/links/0912f51372df672177000000.pdf}, volume = {61}, year = {2007} } @article{Strobel2007, abstract = {Abstract Although it is widely accepted that serotonin plays a pivotal role in the modulation of anxiety- and depression-related personality traits as well as in the pathogenesis of anxiety disorders and depression, the role of serotonin in cognition is less clear. In the present study, we investigated the involvement of serotonin in cognitive behaviors by examining the impact of genetic variation in key regulators of serotonergic neurotransmission on behavioral measures in a cognitive control task. Eighty-five healthy participants performed a cued continuous performance task (the AX Continuous Performance Task [AXCPT]) and were genotyped for polymorphisms in the transcriptional control regions of the tryptophan hydroxylase 2 gene (TPH2 G-703T; rs4570625) and the serotonin transporter gene (5-HTTLPR). The core result was that individuals lacking the rare TPH2 T allele were not faster than T allele carriers, but committed fewer errors and were less variable in responding. These findings parallel those of a recent study where an enhancement of executive control in individuals without the rare TPH2 T/T genotype was observed. Together with recent evidence that individuals without the T allele exhibit higher scores in anxiety- and depression-related personality traits, our results underscore the role of the TPH2 G-703T polymorphism in the modulation of behavior and raise the intriguing possibility that genetic variants associated with higher negative emotionality may have beneficial effects on some cognitive functions.}, author = {Strobel, Alexander and Dreisbach, Gesine and Müller, Johannes and Goschke, Thomas and Brocke, Burkhard and Lesch, Klaus-Peter}, doi = {10.1162/jocn.2007.19.12.1923}, journal = {The Journal of Cognitive Neuroscience}, month = {jan}, pages = {080219115128817-9}, title = {Genetic variation of serotonin function and cognitive control}, url = {https://oadoi.org/10.1162/jocn.2007.19.12.1923}, volume = {Early Access}, year = {2007} } @article{Trigo2007, author = {Trigo, José Manuel and Renoir, Thibault and Lanfumey, Laurence and Hamon, Michel and Lesch, Klaus-Peter and Robledo, Patricia and Maldonado, Rafael}, doi = {10.1016/j.biopsych.2006.11.005}, journal = {Biological Psychiatry}, month = {sep}, pages = {669-679}, title = {3,4-Methylenedioxymethamphetamine Self-Administration is Abolished in Serotonin Transporter Knockout Mice}, url = {https://oadoi.org/10.1016/j.biopsych.2006.11.005}, volume = {62}, year = {2007} }