Karch, André

[["dc.bibliographiccitation.firstpage","1013"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","1023"],["dc.bibliographiccitation.volume","129"],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","Deeg, S."],["dc.contributor.author","Voigt, A."],["dc.contributor.author","Voßfeldt, H."],["dc.contributor.author","Dohm, C. P."],["dc.contributor.author","Karch, A."],["dc.contributor.author","Weishaupt, Jochen"],["dc.contributor.author","Schulz, J. B."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Kermer, P."],["dc.date.accessioned","2017-09-07T11:46:13Z"],["dc.date.available","2017-09-07T11:46:13Z"],["dc.date.issued","2014"],["dc.description.abstract","Spinocerebellar ataxia type 3 (SCA3) is one of at least nine inherited neurodegenerative diseases caused by an expansion of a polyglutamine tract within corresponding disease-specific proteins. In case of SCA3, mutation of Ataxin-3 results in aggregation of misfolded protein, formation of intranuclear as well as cytosolic inclusion bodies and cell death in distinct neuronal populations. Since cyclin-dependent kinase-5 (CDK5) has been shown to exert beneficial effects on aggregate formation and cell death in various polyglutamine diseases, we tested its therapeutic potential for SCA3. Our data show increased caspase-dependent Ataxin-3 cleavage, aggregation, and neurodegeneration in the absence of sufficient CDK5 activity. This disease-propagating effect could be reversed by mutation of the caspase cleavage site in Ataxin-3. Moreover, reduction of CDK5 expression levels by RNAi in vivo enhances SCA3 toxicity as assayed in a Drosophila model for SCA3. In summary, we present CDK5 as a potent neuroprotectant, regulating cleavage and thereby toxicity of Ataxin-3 and other polyglutamine proteins. We propose that increased caspase-dependent cleavage of mutated Ataxin-3, because of missing CDK5 shielding, leads to aggregation and cell death. Moreover, reduction of CDK5 expression levels by RNAi in vivo enhances SCA3 toxicity as assayed in a Drosophila model for SCA3. We think that CDK5 functions as a shield against cleavage-induced toxification and thereby is an interesting target for therapeutic intervention in polyQ disease in general."],["dc.identifier.doi","10.1111/jnc.12684"],["dc.identifier.gro","3142111"],["dc.identifier.isi","000337760500011"],["dc.identifier.pmid","24548080"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/4666"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1471-4159"],["dc.relation.issn","0022-3042"],["dc.title","CDK5 protects from caspase-induced Ataxin-3 cleavage and neurodegeneration"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","73"],["dc.bibliographiccitation.journal","Journal of Clinical Epidemiology"],["dc.bibliographiccitation.lastpage","82"],["dc.bibliographiccitation.volume","78"],["dc.contributor.author","Karch, Annika"],["dc.contributor.author","Koch, Armin"],["dc.contributor.author","Zapf, Antonia"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Karch, Andre"],["dc.date.accessioned","2018-11-07T10:07:22Z"],["dc.date.available","2018-11-07T10:07:22Z"],["dc.date.issued","2016"],["dc.description.abstract","Objective: To investigate how choice of gold standard biases estimates of sensitivity and specificity in studies reassessing the diagnostic accuracy of biomarkers that are already part of a lifetime composite gold standard (CGS). Study Design and Setting: We performed a simulation study based on the real-life example of the biomarker \"protein 14-3-3\" used for diagnosing Creutzfeldt Jakob disease. Three different types of gold standard were compared: perfect gold standard \"autopsy\" (available in a small fraction only; prone to partial verification bias), lifetime CGS (including the biomarker under investigation; prone to incorporation bias), and \"best available\" gold standard (autopsy if available, otherwise CGS). Results: Sensitivity was unbiased when comparing 14-3-3 with autopsy but overestimated when using CGS or \"best available\" gold standard. Specificity of 14-3-3 was underestimated in scenarios comparing 14-3-3 with autopsy (up to 24%). In contrast, overestimation (up to 20%) was observed for specificity compared with CGS; this could be reduced to 0-10% when using the \"best available\" gold standard. Conclusion: Choice of gold standard affects considerably estimates of diagnostic accuracy. Using the \"best available\" gold standard (autopsy where available, otherwise CGS) leads to valid estimates of specificity, whereas sensitivity is estimated best when tested against autopsy alone. (C) 2016 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.jclinepi.2016.03.022"],["dc.identifier.isi","000389615400010"],["dc.identifier.pmid","27107877"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39262"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.relation.issn","1878-5921"],["dc.relation.issn","0895-4356"],["dc.title","Partial verification bias and incorporation bias affected accuracy estimates of diagnostic studies for biomarkers that were part of an existing composite gold standard"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","423"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","International Journal of Stroke"],["dc.bibliographiccitation.lastpage","429"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Schnieder, Marlena"],["dc.contributor.author","Siddiqui, Tariq"],["dc.contributor.author","Karch, André"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Schroeter, Marco R"],["dc.contributor.author","Liman, Jan"],["dc.date.accessioned","2020-12-10T18:38:36Z"],["dc.date.available","2020-12-10T18:38:36Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1177/1747493018816511"],["dc.identifier.eissn","1747-4949"],["dc.identifier.issn","1747-4930"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77384"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Low flow in the left atrial appendage assessed by transesophageal echocardiography is associated with increased stroke severity—Results of a single-center cross-sectional study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2189"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Molecular Neurobiology"],["dc.bibliographiccitation.lastpage","2199"],["dc.bibliographiccitation.volume","53"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Ebert, Elisabeth"],["dc.contributor.author","Stoeck, Katharina"],["dc.contributor.author","Karch, Andre"],["dc.contributor.author","Collins, Steven J."],["dc.contributor.author","Calero, Miguel"],["dc.contributor.author","Sklaviadis, Theodor"],["dc.contributor.author","Laplanche, Jean-Louis"],["dc.contributor.author","Golanska, Ewa"],["dc.contributor.author","Baldeiras, Ines"],["dc.contributor.author","Satoh, Katsuya"],["dc.contributor.author","Sanchez-Valle, Raquel"],["dc.contributor.author","Ladogana, Anna"],["dc.contributor.author","Skinningsrud, Anders"],["dc.contributor.author","Hammarin, Anna-Lena"],["dc.contributor.author","Mitrova, Eva"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Kim, Yong Sun"],["dc.contributor.author","Green, Alison"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T10:15:19Z"],["dc.date.available","2018-11-07T10:15:19Z"],["dc.date.issued","2016"],["dc.description.abstract","At present, the testing of 14-3-3 protein in cerebrospinal fluid (CSF) is a standard biomarker test in suspected sporadic Creutzfeldt-Jakob disease (sCJD) diagnosis. Increasing 14-3-3 test referrals in CJD reference laboratories in the last years have led to an urgent need to improve established 14-3-3 test methods. The main result of our study was the validation of a commercially available 14-3-3 ELISA next to the commonly used Western blot method as a high-throughput screening test. Hereby, 14-3-3 protein expression was quantitatively analyzed in CSF of 231 sCJD and 2035 control patients. We obtained excellent sensitivity/specificity values of 88 and 96 % that are comparable to the established Western blot method. Since standard protocols and preanalytical sample handling have become more important in routine diagnostic, we investigated in a further step the reproducibility and stability of 14-3-3 as a biomarker for human prion diseases. Ring trial data from 2009 to 2013 revealed an increase of Fleiss' kappa from 0.51 to 0.68 indicating an improving reliability of 14-3-3 protein detection. The stability of 14-3-3 protein under short-term and long-term storage conditions at various temperatures and after repeated freezing/thawing cycles was confirmed. Contamination of CSF samples with blood appears likely to be an important factor at a concentration of more than 2500 erythrocytes/mu L. Hemolysis of erythrocytes with significant release of 14-3-3 protein started after 2 days at room temperature. We first define clear standards for the sample handling, short- and long-term storage of CSF samples as well as the handling of blood- contaminated samples which may result in artificially elevated CSF levels of 14-3-3."],["dc.identifier.doi","10.1007/s12035-015-9167-5"],["dc.identifier.isi","000373641500011"],["dc.identifier.pmid","25947081"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40787"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Humana Press Inc"],["dc.relation.issn","1559-1182"],["dc.relation.issn","0893-7648"],["dc.title","Validation of 14-3-3 Protein as a Marker in Sporadic Creutzfeldt-Jakob Disease Diagnostic"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1182"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Stroke"],["dc.bibliographiccitation.lastpage","1189"],["dc.bibliographiccitation.volume","51"],["dc.contributor.author","Sporns, Peter B."],["dc.contributor.author","Straeter, Ronald"],["dc.contributor.author","Minnerup, Jens"],["dc.contributor.author","Wiendl, Heinz"],["dc.contributor.author","Hanning, Uta"],["dc.contributor.author","Chapot, René"],["dc.contributor.author","Henkes, Hans"],["dc.contributor.author","Henkes, Elina"],["dc.contributor.author","Grams, Astrid"],["dc.contributor.author","Dorn, Franziska"],["dc.contributor.author","Nikoubashman, Omid"],["dc.contributor.author","Wiesmann, Martin"],["dc.contributor.author","Bier, Georg"],["dc.contributor.author","Weber, Anushe"],["dc.contributor.author","Broocks, Gabriel"],["dc.contributor.author","Fiehler, Jens"],["dc.contributor.author","Brehm, Alex"],["dc.contributor.author","Psychogios, Marios"],["dc.contributor.author","Kaiser, Daniel"],["dc.contributor.author","Yilmaz, Umut"],["dc.contributor.author","Morotti, Andrea"],["dc.contributor.author","Marik, Wolfgang"],["dc.contributor.author","Nolz, Richard"],["dc.contributor.author","Jensen-Kondering, Ulf"],["dc.contributor.author","Schmitz, Bernd"],["dc.contributor.author","Schob, Stefan"],["dc.contributor.author","Beuing, Oliver"],["dc.contributor.author","Goetz, Friedrich"],["dc.contributor.author","Trenkler, Johannes"],["dc.contributor.author","Turowski, Bernd"],["dc.contributor.author","Möhlenbruch, Markus"],["dc.contributor.author","Wendl, Christina"],["dc.contributor.author","Schramm, Peter"],["dc.contributor.author","Musolino, Patricia"],["dc.contributor.author","Lee, Sarah"],["dc.contributor.author","Schlamann, Marc"],["dc.contributor.author","Radbruch, Alexander"],["dc.contributor.author","Rübsamen, Nicole"],["dc.contributor.author","Karch, André"],["dc.contributor.author","Heindel, Walter"],["dc.contributor.author","Wildgruber, Moritz"],["dc.contributor.author","Kemmling, André"],["dc.date.accessioned","2020-12-10T18:38:10Z"],["dc.date.available","2020-12-10T18:38:10Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1161/STROKEAHA.119.028221"],["dc.identifier.eissn","1524-4628"],["dc.identifier.issn","0039-2499"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77204"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Does Device Selection Impact Recanalization Rate and Neurological Outcome?"],["dc.title.alternative","An Analysis of the Save ChildS Study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","71"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Dementia and Geriatric Cognitive Disorders"],["dc.bibliographiccitation.lastpage","80"],["dc.bibliographiccitation.volume","43"],["dc.contributor.author","Llorens, Franc"],["dc.contributor.author","Karch, Andre"],["dc.contributor.author","Golanska, Ewa"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Lange, Peter"],["dc.contributor.author","Sikorska, Beata"],["dc.contributor.author","Liberski, Pawel P."],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T10:28:45Z"],["dc.date.available","2018-11-07T10:28:45Z"],["dc.date.issued","2017"],["dc.description.abstract","Background: Several biomarkers have been proposed to discriminate sporadic Creutzfeldt-Jakob disease (sCJD) from other dementias and control cases. However, their clinical accuracy depends on the PRNP codon 129 genotype, leaving it unclear how well established markers behave in untested conditions. Methods: We analyzed 14-3-3, tau, p-tau levels, and the p-tau/ tau ratio in a population sample collected from Polish hospitals including nondementia, dementia, and definite sCJD cases and validated their parameters according to previously established cutoffs. Additionally, the correlation between biomarkers and disease duration as well as the influence of the PRNP129 polymorphism are reported. Results: The tau levels and p-tau/tau ratios differed considerably between sCJD and clinically characterized non-CJD cases (p < 0.001). p-tau was only elevated in sCJD when compared to cases without dementia (p < 0.05). Tau and the p-tau/tau ratio showed a sensitivity of 95 and 100%, respectively, in detecting sCJD cases. A negative correlation between tau levels and disease duration, but not the timing of lumbar puncture was observed. Conclusion: The present findings confirmed the value of the p-tau/tau ratio as a robust sCJD biomarker and suggest a role for tau as prognostic marker. (C) 2017 S. Karger AG, Basel."],["dc.identifier.doi","10.1159/000454802"],["dc.identifier.isi","000395664800007"],["dc.identifier.pmid","28056460"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43497"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Karger"],["dc.relation.issn","1421-9824"],["dc.relation.issn","1420-8008"],["dc.title","Cerebrospinal Fluid Biomarker-Based Diagnosis of Sporadic Creutzfeldt-Jakob Disease: A Validation Study for Previously Established Cutoffs"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","451"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Alzheimer s Disease"],["dc.bibliographiccitation.lastpage","454"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Schmidt, Christian D."],["dc.contributor.author","Karch, Andre"],["dc.contributor.author","Artjomova, Svetlana"],["dc.contributor.author","Hoeschel, Martin"],["dc.contributor.author","Zerr, Inga"],["dc.date.accessioned","2018-11-07T09:30:00Z"],["dc.date.available","2018-11-07T09:30:00Z"],["dc.date.issued","2013"],["dc.description.abstract","Background: Pre-progression rates (PPR) in Alzheimer's disease (AD) have been reported to be associated with cognitive and functional decline. Objective: The objective was to reevaluate PPRs in a prospective cohort of AD patients. Methods: A prospective AD cohort was analyzed. Multiple regression was used to examine associations of PPRs with short term decline on different cognitive and functional scales (MMSE, instrumental and basic ADL, GDS, UPDRS III). Results: PPRs were only associated with first year instrumental ADL declines. Conclusion: The predictive abilities of PPRs could partially be confirmed. These findings can help to adapt patient care shortly after diagnosis."],["dc.identifier.doi","10.3233/JAD-130074"],["dc.identifier.isi","000318627800003"],["dc.identifier.pmid","23435410"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31196"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Ios Press"],["dc.relation.issn","1387-2877"],["dc.title","Pre-Progression Rates in Alzheimer's Disease Revisited"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","264"],["dc.bibliographiccitation.issue","5-6"],["dc.bibliographiccitation.journal","European Neurology"],["dc.bibliographiccitation.lastpage","269"],["dc.bibliographiccitation.volume","78"],["dc.contributor.author","Schnieder, Marlena"],["dc.contributor.author","Siddiqui, Tariq"],["dc.contributor.author","Karch, André"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","Schroeter, Marco R."],["dc.contributor.author","Hasenfuss, Gerd"],["dc.date.accessioned","2018-04-23T11:49:25Z"],["dc.date.available","2018-04-23T11:49:25Z"],["dc.date.issued","2017"],["dc.description.abstract","Background: A significant proportion of ischemic strokes are cryptogenic. In this context, the clinical pertinence of patent foramen ovale (PFO) with and without atrial septum aneurysm (ASA) remains controversial. The aim of this study was to identify how PFO +/–ASA and cryptogenic stroke are associated in a representative sample of stroke patients. Methods: We enrolled all patients (n = 909) with ischemic stroke or transient ischemic attack admitted to the certified stroke unit or neurological intensive care unit of our university medical center who underwent transesophageal echocardiography (TEE) between 2012 and 2014. The baseline characteristics, cardio-/neurovascular risk factors, clinical parameters and TEE findings were analyzed. Results: PFO was present in 26.2%, and PFO was combined with an ASA in 9.9%. In cryptogenic stroke, the prevalence of PFO was higher compared to other etiologies (30.9 vs. 21.9%; p < 0.002). Patients with PFO had lower National Institute of Health Stroke Score (NIHSS) values at admission than those without (2 [0–5] vs. 3 [1–7]; p = 0.001; 95% CI [0.62–0.88]). No difference was found in NIHSS values of PFO patients with or without ASA (2 [0–5] vs. 2 [0–5]; p = 0.683; 95% CI 0.94 [0.68–1.28]). Conclusions: Our study indicates that a detected PFO +/–ASA could exhibit a stroke-relevant finding, if classical risk factors for the stroke were lacking."],["dc.identifier.doi","10.1159/000479962"],["dc.identifier.gro","3142067"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/13691"],["dc.language.iso","en"],["dc.notes.intern","lifescience updates Crossref Import"],["dc.notes.status","final"],["dc.relation.issn","0014-3022"],["dc.title","Clinical Relevance of Patent Foramen Ovale and Atrial Septum Aneurysm in Stroke: Findings of a Single-Center Cross-Sectional Study"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","25"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","JAMA Neurology"],["dc.bibliographiccitation.volume","77"],["dc.contributor.author","Sporns, Peter B."],["dc.contributor.author","Sträter, Ronald"],["dc.contributor.author","Minnerup, Jens"],["dc.contributor.author","Wiendl, Heinz"],["dc.contributor.author","Hanning, Uta"],["dc.contributor.author","Chapot, René"],["dc.contributor.author","Henkes, Hans"],["dc.contributor.author","Henkes, Elina"],["dc.contributor.author","Grams, Astrid"],["dc.contributor.author","Dorn, Franziska"],["dc.contributor.author","Nikoubashman, Omid"],["dc.contributor.author","Wiesmann, Martin"],["dc.contributor.author","Bier, Georg"],["dc.contributor.author","Weber, Anushe"],["dc.contributor.author","Broocks, Gabriel"],["dc.contributor.author","Fiehler, Jens"],["dc.contributor.author","Brehm, Alex"],["dc.contributor.author","Psychogios, Marios"],["dc.contributor.author","Kaiser, Daniel"],["dc.contributor.author","Yilmaz, Umut"],["dc.contributor.author","Morotti, Andrea"],["dc.contributor.author","Marik, Wolfgang"],["dc.contributor.author","Nolz, Richard"],["dc.contributor.author","Jensen-Kondering, Ulf"],["dc.contributor.author","Schmitz, Bernd"],["dc.contributor.author","Schob, Stefan"],["dc.contributor.author","Beuing, Oliver"],["dc.contributor.author","Götz, Friedrich"],["dc.contributor.author","Trenkler, Johannes"],["dc.contributor.author","Turowski, Bernd"],["dc.contributor.author","Möhlenbruch, Markus"],["dc.contributor.author","Wendl, Christina"],["dc.contributor.author","Schramm, Peter"],["dc.contributor.author","Musolino, Patricia"],["dc.contributor.author","Lee, Sarah"],["dc.contributor.author","Schlamann, Marc"],["dc.contributor.author","Radbruch, Alexander"],["dc.contributor.author","Rübsamen, Nicole"],["dc.contributor.author","Karch, André"],["dc.contributor.author","Heindel, Walter"],["dc.contributor.author","Wildgruber, Moritz"],["dc.contributor.author","Kemmling, André"],["dc.date.accessioned","2020-12-10T14:05:39Z"],["dc.date.available","2020-12-10T14:05:39Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1001/jamaneurol.2019.3403"],["dc.identifier.issn","2168-6149"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/69606"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Feasibility, Safety, and Outcome of Endovascular Recanalization in Childhood Stroke"],["dc.title.alternative","The Save ChildS Study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1643"],["dc.bibliographiccitation.issue","18"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","1652"],["dc.bibliographiccitation.volume","82"],["dc.contributor.author","Karch, Andre"],["dc.contributor.author","Thomas, Sara L."],["dc.date.accessioned","2018-11-07T09:40:20Z"],["dc.date.available","2018-11-07T09:40:20Z"],["dc.date.issued","2014"],["dc.description.abstract","Objective:To investigate the effect of autoimmune thyroiditis (AIT) on risk of stroke and to assess whether any increased risk (1) varied by AIT duration, and (2) was independent of classic cardiovascular risk factors.Methods:This was a large historical cohort study using data from The Health Improvement Network Database. Rates of first stroke during follow-up in thyroxine-treated patients with AIT (n = 34,907) were compared with those in matched individuals without AIT (n = 149,632) using random-effects Poisson regression models.Results:There was strong evidence for a slightly increased risk of stroke in patients with AIT (adjusted rate ratio = 1.10, 95% confidence interval: 1.01-1.20). The observed increase was partly independent of cardiovascular risk factors. Higher effect sizes were identified in the first year after AIT diagnosis (rate ratio = 1.33, 95% confidence interval: 1.14-1.56) but not in the long-term, consistent with a residual effect of hypothyroidism.Conclusion:Our results support the hypothesis of a slightly increased risk of stroke in patients with AIT. The higher effect size found soon after AIT diagnosis suggests an increased cardiovascular risk due to thyroid-hormone deficiency rather than a cumulative effect of autoimmune pathology. Better screening and early treatment of patients with asymptomatic hypothyroid AIT could help reduce excess risk of stroke in the first year after diagnosis."],["dc.description.sponsorship","Wellcome Trust [079482/Z/06/Z]; DAAD (German Academic Exchange Service)"],["dc.identifier.doi","10.1212/WNL.0000000000000377"],["dc.identifier.isi","000336497400015"],["dc.identifier.pmid","24719488"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33485"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","1526-632X"],["dc.relation.issn","0028-3878"],["dc.title","Autoimmune thyroiditis as a risk factor for stroke A historical cohort study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]