Falkai, Peter Gaston

[["dc.bibliographiccitation.firstpage","1651"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of Neural Transmission"],["dc.bibliographiccitation.lastpage","1659"],["dc.bibliographiccitation.volume","115"],["dc.contributor.author","Kessler, Holger"],["dc.contributor.author","Pajonk, Frank-Gerald"],["dc.contributor.author","Bach, Daniela"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Herrmann, Wolfgang"],["dc.contributor.author","Multhaup, Gerd"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Schäfer, Stephanie"],["dc.contributor.author","Wirths, Oliver"],["dc.contributor.author","Bayer, Thomas"],["dc.date.accessioned","2019-07-09T11:52:23Z"],["dc.date.available","2019-07-09T11:52:23Z"],["dc.date.issued","2008"],["dc.description.abstract","A plethora of reports suggest that copper (Cu) homeostasis is disturbed in Alzheimer’s disease (AD). In the present report we evaluated the efficacy of oral Cu supplementation on Cp. biomarkers for AD. In a prospective, randomized, double-blind, placebo-controlled phase 2 clinical trial (12 months long) patients with mild AD received either Cu-(II)-orotate-dihydrate (verum group; 8 mg Cu daily) or placebo (placebo group). The primary outcome measures in CSF were Aβ42, Tau and Phospho-Tau. The clinical trial demonstrates that long-term oral intake of 8 mg Cu can be excluded as a risk factor for AD based on CSF biomarker analysis. Cu intake had no effect on the progression of Tau and Phospho-Tau levels in CSF. While Aβ42 levels declined by 30% in the placebo group (P = 0.001), they decreased only by 10% (P = 0.04) in the verum group. Since decreased CSF Aβ42 is a diagnostic marker for AD, this observation may indicate that Cu treatment had a positive effect on a relevant AD biomarker. Using mini-mental state examination (MMSE) and Alzheimer disease assessment scale-cognitive subscale (ADAS-cog) we have previously demonstrated that there are no Cu treatment effects on cognitive performance, however. Finally, CSF Aβ42 levels declined significantly in both groups within 12 months supporting the notion that CSF Aβ42 may be valid not only for diagnostic but also for prognostic purposes in AD."],["dc.identifier.doi","10.1007/s00702-008-0136-2"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/3561"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60172"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Springer"],["dc.publisher.place","Vienna"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Effect of copper intake on CSF parameters in patients with mild Alzheimer’s disease: a pilot phase 2 clinical trial"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","91"],["dc.bibliographiccitation.journal","BMC Psychiatry"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Ribbe, Katja"],["dc.contributor.author","Friedrichs, Heidi"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Grube, Sabrina"],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Kästner, Anne"],["dc.contributor.author","Gerchen, Martin Fungisai"],["dc.contributor.author","Ackermann, Verena"],["dc.contributor.author","Tarami, Asieh"],["dc.contributor.author","Treitz, Annika"],["dc.contributor.author","Flögel, Marlene"],["dc.contributor.author","Adler, Lothar"],["dc.contributor.author","Aldenhoff, Josef B."],["dc.contributor.author","Becker-Emner, Marianne"],["dc.contributor.author","Becker, Thomas"],["dc.contributor.author","Czernik, Adelheid"],["dc.contributor.author","Dose, Matthias"],["dc.contributor.author","Folkerts, Here"],["dc.contributor.author","Freese, Roland"],["dc.contributor.author","Guenther, Rolf"],["dc.contributor.author","Herpertz, Sabine"],["dc.contributor.author","Hesse, Dirk"],["dc.contributor.author","Kruse, Gunther"],["dc.contributor.author","Kunze, Heinrich"],["dc.contributor.author","Franz, Michael"],["dc.contributor.author","Lohrer, Frank"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Mielke, Andreas"],["dc.contributor.author","Müller-Isberner, Rüdiger"],["dc.contributor.author","Oestereich, Cornelia"],["dc.contributor.author","Pajonk, Frank-Gerald"],["dc.contributor.author","Pollmächer, Thomas"],["dc.contributor.author","Schneider, Udo"],["dc.contributor.author","Schwarz, Hans-Joachim"],["dc.contributor.author","Kröner-Herwig, Birgit"],["dc.contributor.author","Havemann-Reinecke, Ursula"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Stühmer, Walter"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:37Z"],["dc.date.available","2017-09-07T11:46:37Z"],["dc.date.issued","2010"],["dc.description.abstract","Background: Schizophrenia is the collective term for an exclusively clinically diagnosed, heterogeneous group of mental disorders with still obscure biological roots. Based on the assumption that valuable information about relevant genetic and environmental disease mechanisms can be obtained by association studies on patient cohorts of ≥ 1000 patients, if performed on detailed clinical datasets and quantifiable biological readouts, we generated a new schizophrenia data base, the GRAS (Göttingen Research Association for Schizophrenia) data collection. GRAS is the necessary ground to study genetic causes of the schizophrenic phenotype in a 'phenotype-based genetic association study' (PGAS). This approach is different from and complementary to the genome-wide association studies (GWAS) on schizophrenia. Methods: For this purpose, 1085 patients were recruited between 2005 and 2010 by an invariable team of traveling investigators in a cross-sectional field study that comprised 23 German psychiatric hospitals. Additionally, chart records and discharge letters of all patients were collected. Results: The corresponding dataset extracted and presented in form of an overview here, comprises biographic information, disease history, medication including side effects, and results of comprehensive cross-sectional psychopathological, neuropsychological, and neurological examinations. With >3000 data points per schizophrenic subject, this data base of living patients, who are also accessible for follow-up studies, provides a wide-ranging and standardized phenotype characterization of as yet unprecedented detail. Conclusions: The GRAS data base will serve as prerequisite for PGAS, a novel approach to better understanding 'the schizophrenias' through exploring the contribution of genetic variation to the schizophrenic phenotypes."],["dc.format.extent","20"],["dc.identifier.doi","10.1186/1471-244X-10-91"],["dc.identifier.gro","3150558"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5803"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7333"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","The cross-sectional GRAS sample: a comprehensive phenotypical data collection of schizophrenic patients"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","133"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","ARCH GEN PSYCHIATRY"],["dc.bibliographiccitation.lastpage","143"],["dc.bibliographiccitation.volume","67"],["dc.contributor.author","Pajonk, Frank-Gerald"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Scherk, Harald"],["dc.contributor.author","Berner, Dorothea"],["dc.contributor.author","Kaizl, Inge"],["dc.contributor.author","Kierer, Astrid"],["dc.contributor.author","Müller, Stephanie"],["dc.contributor.author","Oest, Martin"],["dc.contributor.author","Meyer, Tim"],["dc.contributor.author","Backens, Martin"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Thornton, Allen E."],["dc.contributor.author","Honer, Willam G."],["dc.contributor.author","Falkai, Peter"],["dc.date.accessioned","2019-07-10T08:13:32Z"],["dc.date.available","2019-07-10T08:13:32Z"],["dc.date.issued","2010"],["dc.description.abstract","Context: Hippocampal volume is lower than expected in patients with schizophrenia; however, whether this represents a fixed deficit is uncertain. Exercise is a stimulus to hippocampal plasticity. Objective: To determine whether hippocampal volume would increase with exercise in humans and whether this effect would be related to improved aerobic fitness. Design: Randomized controlled study. Setting: Patients attending a day hospital program or an outpatient clinic. Patients or Other Participants: Male patients with chronic schizophrenia and matched healthy subjects. Interventions: Aerobic exercise training (cycling) and playing table football (control group) for a period of 3 months. Main Outcome Measures: Magnetic resonance imaging of the hippocampus. Secondary outcome measures were magnetic resonance spectroscopy, neuropsychological (Rey Auditory Verbal Learning Test, Corsi blocktapping test), and clinical (Positive and Negative Syndrome Scale) features. Results: Following exercise training, relative hippocampal volume increased significantly in patients (12%) and healthy subjects (16%), with no change in the nonexercise group of patients (−1%). Changes in hippocampal volume in the exercise group were correlated with improvements in aerobic fitness measured by change in maximum oxygen consumption (r=0.71; P=.003). In the schizophrenia exercise group (but not the controls), change in hippocampal volume was associated with a 35% increase in the N-acetylaspartate to creatine ratio in the hippocampus. Finally, improvement in test scores for short-term memory in the combined exercise and nonexercise schizophrenia group was correlated with change in hippocampal volume (r=0.51; P .05). Conclusion: These results indicate that in both healthy subjects and patients with schizophrenia hippocampal volume is plastic in response to aerobic exercise."],["dc.identifier.fs","575536"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6145"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/61270"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Hippocampal Plasticity in Response to Exercise in Schizophrenia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]