Windl, Otto

[["dc.bibliographiccitation.firstpage","2558"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","2566"],["dc.bibliographiccitation.volume","125"],["dc.contributor.author","Tschampa, Henriette J."],["dc.contributor.author","Herms, J. W."],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Maruschak, B."],["dc.contributor.author","Windl, Otto"],["dc.contributor.author","Jastrow, U."],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Steinhoff, B. J."],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.date.accessioned","2018-11-07T09:51:28Z"],["dc.date.available","2018-11-07T09:51:28Z"],["dc.date.issued","2002"],["dc.description.abstract","The pathogenesis underlying the typical findings in Creutzfeldt-Jakob disease (CJD) such as periodic EEG changes or myoclonus is not fully understood. The thalamus possesses a high density of inhibitory neurones and serves as a crucial pacemaker of rhythmic EEG activity. As inhibitory neurones expressing parvalbumin (PV) are reduced in the cerebral cortex and hippocampus in sporadic CJD (sCJD), we studied the distribution and number of PV-immunoreactive neurones in sCJD thalami in order to determine whether damage to them could account for certain clinical findings. Immuno histochemical analysis was performed on the thalami from 21 sCJD patients and five controls. The number of PV+ neurones was counted in the thalamic nuclei and compared with clinical and molecular findings. In sCJD patients, PV+ neurones were significantly reduced in the ventrolateral posterior (VLp), ventrolateral anterior (VLa), anteroventral (AV), lateral dorsal (LD), mediodorsal (MD) and reticular (Re) thalamic nuclei (P < 0.05). The VLp was especially damaged in sCJD patients with homozygosity for methionine at codon 129 and scrapie prion protein (PrPSc) type 1. Patients with typical EEG changes [periodic sharp wave complexes (PSWCs)] and myoclonus had a predominant loss of PV+ cells in the reticular thalamic nucleus. In conclusion, our data support the hypothesis that the damage to PV-immunoreactive neurones determines the generation of certain typical clinical features of CJD, i.e. PSWCs associated with myoclonus."],["dc.identifier.doi","10.1093/brain/awf253"],["dc.identifier.isi","000178834400016"],["dc.identifier.pmid","12390980"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35920"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.title","Clinical findings in sporadic Creutzfeldt-Jakob disease correlate with thalamic pathology"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","32"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","40"],["dc.bibliographiccitation.volume","43"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Bodemer, Monika"],["dc.contributor.author","Gefeller, Olaf"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Windl, Otto"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Weber, Thomas"],["dc.date.accessioned","2017-09-07T11:44:31Z"],["dc.date.available","2017-09-07T11:44:31Z"],["dc.date.issued","1998"],["dc.description.abstract","The analysis of 14-3-3 protein in cerebrospinal fluid (CSF) was shown to be highly sensitive and specific for the diagnosis of Creutzfeldt-Jakob disease (CJD). However, the predictive value of this test in the clinical diagnosis of, and its relation to, sporadic, genetic, and iatrogenic CJD cases have yet to be established. CSF samples of suspect CJD cases seen in the prospective German surveillance study were tested for the presence of 14-3-3 protein by using a modified western blot (WB) technique. WB detected 14-3-3 protein in 95.4% of definite and 92.8% of probable cases. In two patients classified initially as not having CJD the test was positive, and both were later proved to have definite CJD. The positive predictive value is 94.7% and the negative predictive value is 92.4%. False-positive results in a single CSF analysis were seen in patients with herpes simplex encephalitis, hypoxic brain damage, atypical encephalitis, intracerebral metastases of a bronchial carcinoma, metabolic encephalopathy, and progressive dementia of unknown cause. WB analysis for 14-3-3 protein was positive in only 5 of 10 cases of familial forms of spongiform encephalopathies. CSF analysis for 14-3-3 protein should thus be performed in any case suspect for CJD."],["dc.identifier.doi","10.1002/ana.410430109"],["dc.identifier.gro","3151695"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8514"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0364-5134"],["dc.title","Detection of 14-3-3 protein in the cerebrospinal fluid supports the diagnosis of Creutzfeldt-Jakob disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","450"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","456"],["dc.bibliographiccitation.volume","63"],["dc.contributor.author","Meissner, Bettina"],["dc.contributor.author","Kohler, K."],["dc.contributor.author","Kortner, K."],["dc.contributor.author","Bartl, Mario"],["dc.contributor.author","Jastrow, U."],["dc.contributor.author","Mollenhauer, Brit"],["dc.contributor.author","Schroter, A."],["dc.contributor.author","Finkenstaedt, M."],["dc.contributor.author","Windl, Otto"],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Zerr, I."],["dc.date.accessioned","2018-11-07T10:46:27Z"],["dc.date.available","2018-11-07T10:46:27Z"],["dc.date.issued","2004"],["dc.description.abstract","Objective: To assess if clinical features, prion protein codon 129, and molecular subtype correlate with MRI basal ganglia hyperintensity in sporadic Creutzfeldt-Jakob disease (CJD). Methods: The authors studied 219 patients including 153 confirmed CJD cases for their neurologic symptoms and MRI findings. The MRI was assessed by a blinded investigator for the presence of high signal intensity on T2-weighted images in the basal ganglia. Results: Patients with basal ganglia high signal on T2-weighted images were more likely to present with rapid progressive dementia in an early stage and shorter disease duration (median 6.7 months and 8.6 months). Surprisingly, among the CJD cases, patients without signal increase of the basal ganglia were shown to have a higher frequency of extrapyramidal disturbances (82% vs 70%). More striking differences were found for symptoms such as depression and sensory disturbances, which were more frequent among cases without signal increase. MRI was more likely to be diagnostic in patients with MV2 molecular subtype. Conclusions: Selected clinical and pathologic features correlate with the presence of basal ganglia high signal on T2-weighted MRI in patients with definite or probable CJD."],["dc.identifier.isi","000223229100009"],["dc.identifier.pmid","15314808"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47747"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0028-3878"],["dc.title","Sporadic Creutzfeldt-Jakob disease - Magnetic resonance imaging and clinical findings"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S131"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neurobiology of Aging"],["dc.bibliographiccitation.lastpage","S132"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Ratzka, P."],["dc.contributor.author","Doehlinger, S."],["dc.contributor.author","Boekhoff, I."],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Prange, Hilmar"],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Irle, W."],["dc.contributor.author","Pergande, G."],["dc.contributor.author","Eller-Lenz, B."],["dc.contributor.author","Windl, Otto"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.date.accessioned","2018-11-07T10:23:11Z"],["dc.date.available","2018-11-07T10:23:11Z"],["dc.date.issued","2002"],["dc.identifier.isi","000177465300486"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42407"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.publisher.place","New york"],["dc.relation.issn","0197-4580"],["dc.title","Efficacy of flupirtine on cognitive function in patients with Creutzfeldt-Jakob-disease"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1099"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","1102"],["dc.bibliographiccitation.volume","54"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Esselmann, Herrmann"],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Neumann, M."],["dc.contributor.author","Schroter, A."],["dc.contributor.author","Ratzka, P."],["dc.contributor.author","Cepek, L."],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Windl, Otto"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Wiltfang, J."],["dc.date.accessioned","2018-11-07T08:45:04Z"],["dc.date.available","2018-11-07T08:45:04Z"],["dc.date.issued","2000"],["dc.description.abstract","Objectives: Decreased levels of A beta(1-42) are found in CSF of patients with AD. Because early stages of Creutzfeldt-Jakob disease (CJD) and AD share several clinical features, we investigated A beta(1-42) levels in CSF of these groups, inferring that this might give additional help in differentiating patients with CJD from AD patients. Methods: We investigated 27 patients with CJD, 14 patients with AD, 19 patients with other dementias, and 20 nondemented controls (NDC) for A beta(1-42) in CSF. Twenty-four of the 27 CJD patients were neuropathologically verified. All the neuropathologically verified patients presented with a type 1 prion protein pattern. CJD patients were all homozygous for methionine at codon 129. Except in five CJD patients, no beta-amyloid plaques were seen. Additionally, APOE status was determined in patients with CJD. Results: Levels of A beta(1-42) in CSF were decreased in patients with AD as well as in CJD. Levels of A beta(1-42) in CSF of patients with CJD and AD were significantly different from the other dementia and NDC groups. There was no substantial difference between the CJD and AD groups (p = 0.66). Decreased levels of A beta(1-42) did not correlate with the APOE epsilon 4 load in patients with CJD. Conclusion: Low levels of A beta(1-42) in CSF do not exclude a diagnosis of CJD. Decreased levels of A beta(1-42) in CSF can occur without p-amyloid plaque formation in the brain. However, the underlying mechanism of this phenomenon must be elucidated."],["dc.identifier.isi","000085785700017"],["dc.identifier.pmid","10720281"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20346"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0028-3878"],["dc.title","Decreased beta-amyloid(1-42) in cerebrospinal fluid of patients with Creutzfeldt-Jakob disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","323"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","329"],["dc.bibliographiccitation.volume","48"],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Schulz-Schaeffer, Walter J."],["dc.contributor.author","Giese, A."],["dc.contributor.author","Bodemer, Monika"],["dc.contributor.author","Schroter, A."],["dc.contributor.author","Henkel, K."],["dc.contributor.author","Tschampa, Henriette J."],["dc.contributor.author","Windl, Otto"],["dc.contributor.author","Pfahlberg, Annette"],["dc.contributor.author","Steinhoff, B. J."],["dc.contributor.author","Gefeller, Olaf"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Poser, Sigrid"],["dc.date.accessioned","2018-11-07T10:23:19Z"],["dc.date.available","2018-11-07T10:23:19Z"],["dc.date.issued","2000"],["dc.description.abstract","According to the recently established molecular basis for phenotypic heterogeneity of sporadic Creutzfeldt-Jakob disease (CJD), six different phenotypes are characterized by the size of the protease-resistant fragment of the pathological prion protein (types 1 and 2) and homozygosity or heterozygosity for methionine or valine at codon 129 of the prion protein gene (designated by MM1, MM2, MV1, MV2, VV1, and VV2). In the present investigation, we analyzed the value of commonly used clinical tests (electroencephalogram [EEG], detection of 14-3-3 protein in cerebrospinal fluid [CSF], and hyperintensity of the basal ganglia in magnetic resonance imaging) for the clinical diagnosis in each CJD phenotype. The detection of periodic sharp and slow wave complexes in the EEG is reliable in the clinical diagnosis of MM1 and MV1 patients only. The CSF analysis for 14-3-3 protein showed high sensitivity in all analyzed subgroups with the exception of MV2 patients. Valine-homozygous patients had a negative EEG, but most had detectable levels of neuronal proteins in the CSF. The sensitivity of the magnetic resonance imaging was 70%, irrespective of the subgroup, but was particularly reliable in the clinical diagnosis of MV2 patients. The widening spectrum of diagnostic techniques in CJD is not only useful in the increased accuracy of the clinical diagnosis but should also lead to the identification of more atypical cases of sporadic CJD."],["dc.identifier.doi","10.1002/1531-8249(200009)48:3<323::AID-ANA6>3.0.CO;2-5"],["dc.identifier.isi","000089024600006"],["dc.identifier.pmid","10976638"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42437"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0364-5134"],["dc.title","Current clinical diagnosis in Creutzfeldt-Jakob disease: Identification of uncommon variants"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1099"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Neurology"],["dc.bibliographiccitation.lastpage","1102"],["dc.bibliographiccitation.volume","54"],["dc.contributor.author","Otto, Markus"],["dc.contributor.author","Esselmann, Hermann"],["dc.contributor.author","Schulz-Schaeffer, W."],["dc.contributor.author","Neumann, Manuela"],["dc.contributor.author","Schröter, A."],["dc.contributor.author","Ratzka, P."],["dc.contributor.author","Cepek, L."],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Windl, O."],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Poser, Sigrid"],["dc.contributor.author","Wiltfang, Jens"],["dc.date.accessioned","2017-09-07T11:44:28Z"],["dc.date.available","2017-09-07T11:44:28Z"],["dc.date.issued","2012"],["dc.description.abstract","bjectives: Decreased levels of Aβ1-42 are found in CSF of patients with AD. Because early stages of Creutzfeldt-Jakob disease (CJD) and AD share several clinical features, we investigated Aβ1-42 levels in CSF of these groups, inferring that this might give additional help in differentiating patients with CJD from AD patients.Methods: We investigated 27 patients with CJD, 14 patients with AD, 19 patients with other dementias, and 20 nondemented controls (NDC) for Aβ1-42 in CSF. Twenty-four of the 27 CJD patients were neuropathologically verified. All the neuropathologically verified patients presented with a type 1 prion protein pattern. CJD patients were all homozygous for methionine at codon 129. Except in five CJD patients, no β-amyloid plaques were seen. Additionally, APOE status was determined in patients with CJD.Results: Levels of Aβ1-42 in CSF were decreased in patients with AD as well as in CJD. Levels of Aβ1-42 in CSF of patients with CJD and AD were significantly different from the other dementia and NDC groups. There was no substantial difference between the CJD and AD groups (p = 0.66). Decreased levels of Aβ1-42 did not correlate with the APOE ε4 load in patients with CJD.Conclusion: Low levels of Aβ1-42 in CSF do not exclude a diagnosis of CJD. Decreased levels of Aβ1-42 in CSF can occur without β-amyloid plaque formation in the brain. However, the underlying mechanism of this phenomenon must be elucidated."],["dc.identifier.doi","10.1212/wnl.54.5.1099"],["dc.identifier.gro","3151662"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8479"],["dc.language.iso","en"],["dc.notes.status","public"],["dc.notes.submitter","chake"],["dc.relation.issn","0028-3878"],["dc.title","Decreased  β-amyloid1-42 in cerebrospinal fluid of patients with Creutzfeldt-Jakob disease"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","245"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Brain Pathology"],["dc.bibliographiccitation.lastpage","249"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Sethi, S."],["dc.contributor.author","Foldvari, Z."],["dc.contributor.author","Windl, Otto"],["dc.contributor.author","Querner, V."],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Poser, Sigrid"],["dc.date.accessioned","2018-11-07T10:37:52Z"],["dc.date.available","2018-11-07T10:37:52Z"],["dc.date.issued","2003"],["dc.description.abstract","Florid plaques indistinguishable from those found in vCJD were identified at a postmortem examination in the brain of a 58-year-old clinical suspect case of Creutzfeldt-Jakob disease (CJD). Western blotting of brain tissue revealed an unusual prion protein type. Since the patient had received a dura mater graft 20 years prior to death and florid plaques are not only found in new variant CJD, the findings argue in favor of an iatrogenic origin of the disease with the longest incubation time following a dura mater graft reported to date even though he may have been exposed to BSE. The peculiar pathological, clinical and biochemical features may define a new type of human prion disease."],["dc.identifier.isi","000186614100002"],["dc.identifier.pmid","12946015"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45670"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Int Soc Neuropathology"],["dc.relation.issn","1015-6305"],["dc.title","Latrogenic Creutzfeldt-Jakob disease with florid plaques"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]