Bartels, Claudia

[["dc.bibliographiccitation.journal","Frontiers in Psychiatry"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Hansen, Niels"],["dc.contributor.author","Hirschel, Sina"],["dc.contributor.author","Stöcker, Winfried"],["dc.contributor.author","Manig, Anja"],["dc.contributor.author","Falk, Hannah Sönne"],["dc.contributor.author","Ernst, Marielle"],["dc.contributor.author","Vukovich, Ruth"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Bartels, Claudia"],["dc.date.accessioned","2021-04-14T08:23:48Z"],["dc.date.available","2021-04-14T08:23:48Z"],["dc.date.issued","2020"],["dc.description.abstract","Background IgLON5 disease is an autoimmune disorder that shares neuropathological aspects with a tauopathy. Its clinical spectrum is heterogeneous, and figural memory impairment as an initial phenomenon of IgLON5 syndrome has not yet been described. The rationale of this report is to highlight symptoms related to IgLON5 disease that have not been reported to date. This case report will thereby emphasize how important it is to initiate thorough diagnostic methods including cerebrospinal fluid analysis (CSF) before starting early immunotherapy. Methods We examined a 65-year-old Caucasian male via neuropsychological tests, magnetic resonance imaging (MRI), electroencephalography (EEG), neurography and polysomnography. He also underwent two lumbar punctures from which we determined specific autoantibodies in cerebrospinal (CSF) and peripheral blood (PB). Results The patient presented initially complaining of memory loss, gradual dysphagia and sleeping dysfunction. Neuropsychological testing at first presentation and follow-up revealed subtle figural and working memory impairment. At onset and at his 6-month follow-up, we detected IgLON5 antibodies in CSF and PB. Furthermore, we identified in the CSF a blood–brain barrier disturbance at disease onset and follow-up, and markers of neuroaxonal damage such as mildly elevated phosphorylated Tau-181 protein with 86 pg/ml (normal range ≤ 61 pg/ml) at onset. Three months after his initial presentation, he was suffering from axonal neuropathy and transient ataxia in the extremities. Assuming a definitive autoimmune encephalitis-associated with anti-IgLON5 antibodies, we applied high-dose steroids monthly (1g methylprednisolone i.v. for five consecutive days) and his memory complaints, ataxia of extremities and peripheral neuropathy as well as sleeping dysfunction decreased. Conclusions Our findings broaden IgLON5 disease’s clinical spectrum to include predominant and discrete figural memory impairment together with sleeping dysfunction at disease onset. In addition, our report illustrates how important taking an elaborated diagnostic approach is to assuring an accurate diagnosis and the appropriate therapy if a patient presents with a persisting figural memory impairment and sleeping abnormalities so as to avoid overlooking IgLON5 disease and a potentially poor outcome."],["dc.identifier.doi","10.3389/fpsyt.2020.00576"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17685"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81054"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1664-0640"],["dc.relation.haserratum","/handle/2/83966"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Figural Memory Impairment in Conjunction With Neuropsychiatric Symptoms in IgLON5 Antibody-Associated Autoimmune Encephalitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","The Journal of Clinical Psychiatry"],["dc.bibliographiccitation.volume","81"],["dc.contributor.author","Bartels, Claudia"],["dc.contributor.author","Belz, Michael"],["dc.contributor.author","Vogelgsang, Jonathan"],["dc.contributor.author","Hessmann, Philipp"],["dc.contributor.author","Bohlken, Jens"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Kostev, Karel"],["dc.date.accessioned","2021-04-14T08:32:26Z"],["dc.date.available","2021-04-14T08:32:26Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.4088/JCP.19m13205"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83919"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1555-2101"],["dc.title","To Be Continued? Long-Term Treatment Effects ofAntidepressant Drug Classes and Individual Antidepressants on the Risk of Developing Dementia"],["dc.title.alternative","A German Case-Control Study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e775"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","e788"],["dc.bibliographiccitation.volume","99"],["dc.contributor.author","Billette, Ornella V."],["dc.contributor.author","Ziegler, Gabriel"],["dc.contributor.author","Aruci, Merita"],["dc.contributor.author","Schütze, Hartmut"],["dc.contributor.author","Kizilirmak, Jasmin M."],["dc.contributor.author","Richter, Anni"],["dc.contributor.author","Altenstein, Slawek"],["dc.contributor.author","Bartels, Claudia"],["dc.contributor.author","Brosseron, Frederic"],["dc.contributor.author","Cardenas-Blanco, Arturo"],["dc.contributor.author","Maass, Anne"],["dc.contributor.authorgroup","on behalf of the DELCODE Study Group"],["dc.date.accessioned","2022-09-01T09:50:59Z"],["dc.date.available","2022-09-01T09:50:59Z"],["dc.date.issued","2022"],["dc.description.abstract","Background and Objectives\n We assessed whether novelty-related fMRI activity in medial temporal lobe regions and the precuneus follows an inverted U-shaped pattern across the clinical spectrum of increased Alzheimer disease (AD) risk as previously suggested. Specifically, we tested for potentially increased activity in individuals with a higher AD risk due to subjective cognitive decline (SCD) or mild cognitive impairment (MCI). We further tested whether activity differences related to diagnostic groups were accounted for by CSF markers of AD or brain atrophy.\n \n \n Methods\n We studied 499 participants aged 60–88 years from the German Center for Neurodegenerative Diseases Longitudinal Cognitive Impairment and Dementia Study (DELCODE) who underwent task-fMRI. Participants included 163 cognitively normal (healthy control, HC) individuals, 222 SCD, 82 MCI, and 32 patients with clinical diagnosis of mild AD. CSF levels of β-amyloid 42/40 ratio and phosphorylated-tau181 were available from 232 participants. We used region-based analyses to assess novelty-related activity (novel > highly familiar scenes) in entorhinal cortex, hippocampus, and precuneus as well as whole-brain voxel-wise analyses. First, general linear models tested differences in fMRI activity between participant groups. Complementary regression models tested quadratic relationships between memory impairment and activity. Second, relationships of activity with AD CSF biomarkers and brain volume were analyzed. Analyses were controlled for age, sex, study site, and education.\n \n \n Results\n In the precuneus, we observed an inverted U-shaped pattern of novelty-related activity across groups, with higher activity in SCD and MCI compared with HC, but not in patients with AD who showed relatively lower activity than MCI. This nonlinear pattern was confirmed by a quadratic relationship between memory impairment and precuneus activity. Precuneus activity was not related to AD biomarkers or brain volume. In contrast to the precuneus, hippocampal activity was reduced in AD dementia compared with all other groups and related to AD biomarkers.\n \n \n Discussion\n Novelty-related activity in the precuneus follows a nonlinear pattern across the clinical spectrum of increased AD risk. Although the underlying mechanism remains unclear, increased precuneus activity might represent an early signature of memory impairment. Our results highlight the nonlinearity of activity alterations that should be considered in clinical trials using functional outcome measures or targeting hyperactivity."],["dc.identifier.doi","10.1212/WNL.0000000000200667"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/113848"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-597"],["dc.relation.eissn","1526-632X"],["dc.relation.issn","0028-3878"],["dc.title","Novelty-Related fMRI Responses of Precuneus and Medial Temporal Regions in Individuals at Risk for Alzheimer Disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","92"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Alcohol and Alcoholism"],["dc.bibliographiccitation.lastpage","102"],["dc.bibliographiccitation.volume","42"],["dc.contributor.author","Bartels, Claudia"],["dc.contributor.author","Kunert, Hanns-Jürgen"],["dc.contributor.author","Stawicki, Sabina"],["dc.contributor.author","Kröner-Herwig, Birgit"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Krampe, Henning"],["dc.date.accessioned","2017-09-07T11:46:30Z"],["dc.date.available","2017-09-07T11:46:30Z"],["dc.date.issued","2007"],["dc.description.abstract","The hippocampus (HC) is characterized by high vulnerability to noxious influence, but also by a considerable regenerative potential. Although deficits in HC-related functions are among the most commonly reported cognitive sequelae in alcoholism, little and conflicting information is available concerning regeneration upon abstinence. The present study has been designed to evaluate (i) the frequency of measurable dysfunction in so called HC tests and (ii) its predictive value for risk to relapse in a cohort of 50 severely affected chronic alcoholic patients and (iii) to monitor recovery of HC-related functions upon strict abstention from alcohol. Patients underwent a 2-year neuropsychological follow-up including HC-associated tests (Verbal Learning Test, VLT; Nonverbal Learning Test, NVLT; 'City Map Test' of Learning and Memory Test, LGT-3), as well as tests of intelligence and attention in the framework of OLITA (Outpatient Long-Term Intensive Therapy for Alcoholics), a programme with careful abstinence monitoring. At study entry, 30/50 (60%) alcoholics had HC dysfunction which tended to predict a lower long-term abstinence probability (P = 0.058). Of the subgroup that could be followed under conditions of strictly monitored alcohol abstinence (n = 32; age 44.7 +/- 6.2 years; 23 men, 9 women), 53% (17/32) exhibited distinct HC dysfunction at inclusion which returned to normal after 2 years. Patients with initially normal HC function (9/32) and patients with additional brain damage of different aetiologies (6/32) failed to show improvement on HC-related tests. While the former displayed stably normal HC test performance, the latter remained on a performance level below normal. Demonstrating slow but remarkable regeneration of HC functions upon strict abstention from alcohol, our data strongly support abstinence-oriented long-term treatment of alcoholics. The absence of functional recovery in patients with additional causes of brain damage might be explained by the 'dual hit' exhausting the regenerative potential of the HC."],["dc.identifier.doi","10.1093/alcalc/agl104"],["dc.identifier.gro","3150510"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7282"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","0735-0414"],["dc.title","Recovery of hippocampus-related functions in chronic alcoholics during monitored long-term abstinence"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Archives of Psychiatry and Clinical Neuroscience"],["dc.contributor.author","Belz, Michael"],["dc.contributor.author","Hessmann, Philipp"],["dc.contributor.author","Vogelgsang, Jonathan"],["dc.contributor.author","Schmidt, Ulrike"],["dc.contributor.author","Ruhleder, Mirjana"],["dc.contributor.author","Signerski-Krieger, Jörg"],["dc.contributor.author","Radenbach, Katrin"],["dc.contributor.author","Trost, Sarah"],["dc.contributor.author","Schott, Björn H."],["dc.contributor.author","Bartels, Claudia"],["dc.date.accessioned","2021-06-01T09:42:51Z"],["dc.date.available","2021-06-01T09:42:51Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract The Covid-19 pandemic highly impacts mental health worldwide. Patients with psychiatric disorders are a vulnerable risk population for worsening of their condition and relapse of symptoms. This study investigates the pandemic-related course of psychosocial burden in patients with pre-existing mental disorders. With the newly developed Goettingen psychosocial Burden and Symptom Inventory (Goe-BSI) psychosocial burden has been traced retrospectively (1) before the pandemic (beginning of 2020), (2) at its beginning under maximum lockdown conditions (March 2020), and (3) for the current state after maximum lockdown conditions (April/May 2020). The Goe-BSI also integrates the Adjustment Disorder New Module (ADNM-20), assesses general psychiatric symptoms, and resilience. A total of 213 patients covering all major psychiatric disorders (ICD-10 F0-F9) were interviewed once in the time range from April, 24th until May 11th, 2020. Across all diagnoses patients exhibited a distinct pattern with an initial rise followed by a decline of psychosocial burden ( p  < 0.001, partial η 2  = 0.09; Bonferroni-corrected pairwise comparisons between all three time-points: p  < 0.05 to 0.001). Female gender and high ADNM-20 scores were identified as risk factors for higher levels and an unfavorable course of psychosocial burden over time. Most psychiatric symptoms remained unchanged. Trajectories of psychosocial burden vary in parallel to local lockdown restrictions and seem to reflect an adaptive stress response. For female patients with pre-existing mental disorders and patients with high-stress responses, timely and specific treatment should be scheduled. With the continuation of the pandemic, monitoring of long-term effects is of major importance, especially when long incubation times for the development of mental health issues are considered."],["dc.identifier.doi","10.1007/s00406-021-01268-6"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85373"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1433-8491"],["dc.relation.issn","0940-1334"],["dc.title","Evolution of psychosocial burden and psychiatric symptoms in patients with psychiatric disorders during the Covid-19 pandemic"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e647"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Stroke"],["dc.bibliographiccitation.lastpage","e656"],["dc.bibliographiccitation.volume","40"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Weißenborn, Karin"],["dc.contributor.author","Prange, Hilmar"],["dc.contributor.author","Schneider, Dietmar"],["dc.contributor.author","Weimar, Christian"],["dc.contributor.author","Wartenberg, Katja"],["dc.contributor.author","Schellinger, Peter D."],["dc.contributor.author","Bohn, Matthias"],["dc.contributor.author","Becker, Harald"],["dc.contributor.author","Wegrzyn, Martin"],["dc.contributor.author","Jähnig, Peter"],["dc.contributor.author","Herrmann, Manfred"],["dc.contributor.author","Knauth, Michael"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Heide, Wolfgang"],["dc.contributor.author","Wagner, Armin"],["dc.contributor.author","Schwab, Stefan"],["dc.contributor.author","Reichmann, Heinz"],["dc.contributor.author","Schwendemann, Günther"],["dc.contributor.author","Dengler, Reinhard"],["dc.contributor.author","Kastrup, Andreas"],["dc.contributor.author","Bartels, Claudia"],["dc.date.accessioned","2017-09-07T11:46:20Z"],["dc.date.available","2017-09-07T11:46:20Z"],["dc.date.issued","2009-12"],["dc.description.abstract","Background and Purpose— Numerous preclinical findings and a clinical pilot study suggest that recombinant human erythropoietin (EPO) provides neuroprotection that may be beneficial for the treatment of patients with ischemic stroke. Although EPO has been considered to be a safe and well-tolerated drug over 2 decades, recent studies have identified increased thromboembolic complications and/or mortality risks on EPO administration to patients with cancer or chronic kidney disease. Accordingly, the double-blind, placebo-controlled, randomized German Multicenter EPO Stroke Trial (Phase II/III; ClinicalTrials.gov Identifier: NCT00604630) was designed to evaluate efficacy and safety of EPO in stroke.Methods— This clinical trial enrolled 522 patients with acute ischemic stroke in the middle cerebral artery territory (intent-to-treat population) with 460 patients treated as planned (per-protocol population). Within 6 hours of symptom onset, at 24 and 48 hours, EPO was infused intravenously (40 000 IU each). Systemic thrombolysis with recombinant tissue plasminogen activator was allowed and stratified for.Results— Unexpectedly, a very high number of patients received recombinant tissue plasminogen activator (63.4%). On analysis of total intent-to-treat and per-protocol populations, neither primary outcome Barthel Index on Day 90 (P=0.45) nor any of the other outcome parameters showed favorable effects of EPO. There was an overall death rate of 16.4% (n=42 of 256) in the EPO and 9.0% (n=24 of 266) in the placebo group (OR, 1.98; 95% CI, 1.16 to 3.38; P=0.01) without any particular mechanism of death unexpected after stroke.Conclusions— Based on analysis of total intent-to-treat and per-protocol populations only, this is a negative trial that also raises safety concerns, particularly in patients receiving systemic thrombolysis."],["dc.identifier.doi","10.1161/STROKEAHA.109.564872"],["dc.identifier.gro","3150483"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7252"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.subject","clinical trial; hematopoietic growth factor; neuroprotection; NIHSS; rtPA"],["dc.title","Recombinant Human Erythropoietin in the Treatment of Acute Ischemic Stroke"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Psychiatry"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Hansen, Niels"],["dc.contributor.author","Bartels, Claudia"],["dc.contributor.author","Stöcker, Winfried"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Fitzner, Dirk"],["dc.date.accessioned","2022-04-01T10:00:39Z"],["dc.date.available","2022-04-01T10:00:39Z"],["dc.date.issued","2022"],["dc.description.abstract","Background Glycine receptor antibody-associated neuropsychiatric disease is currently known to be dominated by the phenotypes stiff-person syndrome and progressive encephalomyelitis entailing rigidity and myoclonus. In our case series we aim to depict the less-often reported feature of cognitive impairment associated with glycine receptor antibodies. Methods We investigated five patients with cognitive impairment varying from mild cognitive impairment to dementia associated with serum glycine receptor antibodies. Mild and major neurocognitive disorders were diagnosed according to the DSM-5 (fifth edition of the Diagnostic and Statistical Manual of Mental Disorders). Neuropsychology via Consortium to Establish a Registry for Alzheimer's Disease (CERAD) testing results, psychopathology data via the Manual for the Assessment and Documentation of Psychopathology in Psychiatry (AMDP), cerebrospinal fluid analysis and magnetic resonance imaging data were retrospectively analyzed from patient files. Results We identified five patients with cognitive impairment as the main neuropsychiatric feature associated with serum glycine receptor antibodies. One patient also presented akinetic rigidity syndrome. The psychopathology comprised disorders of attention and memory, orientation, formal thought, and affect. In addition to suffering deficits in verbal memory function, figural recall, phonematic fluency, and globally deteriorated cognitive function, these patients presented seriously impaired memory recall in particular. Tau protein and phosphorylated tau protein 181 were elevated in 75% of patients. Conclusions Our results suggest that axonal neurodegeneration and especially impaired verbal memory recall in addition to deficits in verbal and figural memory characterize patients with progressive cognitive impairment associated with glycine receptor antibodies. This unresolved issue should be clarified by researchers to discover whether axonal degeneration is merely an age-related phenomenon or one related to glycine-receptor autoantibodies in old age. Cognitive impairment as a neuropsychiatric syndrome of glycine-receptor antibody disease is a potential, conceivable, but so far unproven additional feature requiring deeper large-scale investigations and consideration during differential diagnosis in memory clinics."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.3389/fpsyt.2021.778684"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/105481"],["dc.notes.intern","DOI-Import GROB-530"],["dc.relation.eissn","1664-0640"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Impaired Verbal Memory Recall in Patients With Axonal Degeneration and Serum Glycine-Receptor Autoantibodies—Case Series"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","481"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","494"],["dc.bibliographiccitation.volume","139"],["dc.contributor.author","Stuendl, Anne"],["dc.contributor.author","Kunadt, Marcel"],["dc.contributor.author","Kruse, Niels"],["dc.contributor.author","Bartels, Claudia"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Danzer, Karin M."],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Schneider, Anja"],["dc.date.accessioned","2018-11-07T10:18:37Z"],["dc.date.available","2018-11-07T10:18:37Z"],["dc.date.issued","2016"],["dc.description.abstract","Extracellular alpha-synuclein has been proposed as a crucial mechanism for induction of pathological aggregate formation in previously healthy cells. In vitro, extracellular alpha-synuclein is partially associated with exosomal vesicles. Recently, we have provided evidence that exosomal alpha-synuclein is present in the central nervous system in vivo. We hypothesized that exosomal alpha-synuclein species from patients with alpha-synuclein related neurodegeneration serve as carriers for interneuronal disease transmission. We isolated exosomes from cerebrospinal fluid from patients with Parkinson's disease, dementia with Lewy bodies, progressive supranuclear palsy as a non-alpha-synuclein related disorder that clinically overlaps with Parkinson's disease, and neurological controls. Cerebrospinal fluid exosome numbers, alpha-synuclein protein content of cerebrospinal fluid exosomes and their potential to induce oligomerization of alpha-synuclein were analysed. The quantification of cerebrospinal fluid exosomal alpha-synuclein showed distinct differences between patients with Parkinson's disease and dementia with Lewy bodies. In addition, exosomal alpha-synuclein levels correlated with the severity of cognitive impairment in cross-sectional samples from patients with dementia with Lewy bodies. Importantly, cerebrospinal fluid exosomes derived from Parkinson's disease and dementia with Lewy bodies induce oligomerization of alpha-synuclein in a reporter cell line in a dose-dependent manner. Our data suggest that cerebrospinal fluid exosomes from patients with Parkinson's disease and dementia with Lewy bodies contain a pathogenic species of alpha-synuclein, which could initiate oligomerization of soluble alpha-synuclein in target cells and confer disease pathology."],["dc.identifier.doi","10.1093/brain/awv346"],["dc.identifier.isi","000370205100026"],["dc.identifier.pmid","26647156"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/41483"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1460-2156"],["dc.relation.issn","0006-8950"],["dc.title","Induction of alpha-synuclein aggregate formation by CSF exosomes from patients with Parkinson's disease and dementia with Lewy bodies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Multiple Sclerosis Journal"],["dc.contributor.author","Bartels, Claudia"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2018-03-08T09:22:14Z"],["dc.date.available","2018-03-08T09:22:14Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1177/1352458517733132"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/12915"],["dc.language.iso","en"],["dc.notes.intern","GRO-Li-Import"],["dc.notes.status","final"],["dc.relation.doi","10.1177/1352458517733132"],["dc.relation.issn","1352-4585"],["dc.relation.issn","1477-0970"],["dc.title","How to pursue EPO in MS"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","86"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Alcoholism: Clinical and Experimental Research"],["dc.bibliographiccitation.lastpage","95"],["dc.contributor.author","Krampe, Henning"],["dc.contributor.author","Stawicki, Sabina"],["dc.contributor.author","Wagner, Thilo"],["dc.contributor.author","Bartels, Claudia"],["dc.contributor.author","Aust, Carlotta"],["dc.contributor.author","Rüther, Eckart"],["dc.contributor.author","Poser, Wolfgang"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:33Z"],["dc.date.available","2017-09-07T11:46:33Z"],["dc.date.issued","2006"],["dc.description.abstract","Objective: (1) To perform a 9-year study of abstinence, lapse, and relapse in 180 chronic alcoholic patients, participants of the Outpatient Longterm Intensive Therapy for Alcoholics (OLITA); (2) To investigate the role of supervised alcohol deterrents (AD) in relapse prevention and as an adjunct for maintenance of long-term abstinence. Method: This prospective open treatment study evaluates the long-term course of drinking outcomes and AD use of 180 chronic alcoholics consecutively admitted from 1993 to 2002. Subsamples are compared for (1) sham-AD versus verum-AD (disulfiram/calcium carbimide), (2) coped lapses versus finally detrimental lapses versus malignant relapses, and (3) AD use for 13 to 20 versus {.extbackslash}textgreater 20 months. Results: In this 9-year study, the cumulative probability of not having relapsed was 0.52, and that of not having consumed any alcohol was 0.26. Despite long-term use, disulfiram/calcium carbimide was well tolerated. Patients on sham-AD (due to contraindications to verum-AD) showed higher cumulative abstinence probability than patients on verum (S {.extbackslash}textequals 0.86 vs. S {.extbackslash}textequals 0.49, p {.extbackslash}textequals 0.03). Detrimental lapses and malignant relapses occurred earlier than successfully coped lapses (p {.extbackslash}textless 0.001); patients with detrimental lapse and with malignant relapse had rewer days of AD intake and less subsequent days without AD than patients with coped lapse (p {.extbackslash}textless 0.001). The cumulative abstinence probability was S {.extbackslash}textequals 0.75 for patients with long-term intake compared with S {.extbackslash}textequals 0.50 for patients who stopped AD between months 13 and 20 (p {.extbackslash}textless 0.001). Conclusions: An abstinence rate of {.extbackslash}textgreater 50{.extbackslash}textpercent in this 9-year study strongly supports the concept of comprehensive, long-term outpatient treatment of alcoholics. Supervised, guided intake of AD, also over extended periods, can be used as a predominantly psychologically acting ingredient of successful alcoholism therapy."],["dc.identifier.doi","10.1111/j.1530-0277.2006.00013.x"],["dc.identifier.gro","3150523"],["dc.identifier.pmid","16433735"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7295"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.relation.issn","0145-6008"],["dc.title","Follow-up of 180 alcoholic patients for up to 7 years after outpatient treatment: Impact of alcohol deterrents on outcome"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]