Kropp, Stefan

[["dc.bibliographiccitation.firstpage","332"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Acta Neurologica Scandinavica"],["dc.bibliographiccitation.lastpage","334"],["dc.bibliographiccitation.volume","101"],["dc.contributor.author","Bleich, S."],["dc.contributor.author","Kropp, S."],["dc.contributor.author","Degner, D."],["dc.contributor.author","Zerr, I."],["dc.contributor.author","Pilz, J."],["dc.contributor.author","Gleiter, C. H."],["dc.contributor.author","Otto, M."],["dc.contributor.author","Rüther, E."],["dc.contributor.author","Kretzschmar, H. A."],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Kornhuber, J."],["dc.contributor.author","Poser, S."],["dc.date.accessioned","2017-09-07T11:44:36Z"],["dc.date.available","2017-09-07T11:44:36Z"],["dc.date.issued","2000"],["dc.description.abstract","Objectives– Substantial evidence supports the hypothesis that oxygen free radicals are involved in various neurodegenerative disorders. To assess the presence of oxidative stress in Creutzfeldt–Jakob disease (CJD) we examined the concentrations of malondialdehyde (MDA) as an established marker of lipid peroxidation. Material and methods– MDA was quantified by high performance liquid chromatography (HPLC) in cerebrospinal fluid (CSF; n=12) and in serum (n=11) samples of CJD patients and healthy controls (n=15). Results– Mean values in healthy controls: 2.56 nmol/ml±0.46 (CSF) and 1.94 nmol/ml±0.67 (serum); mean values in CJD patients: 2.64 nmol/ml±0.67 (CSF) and 1.68 nmol/ml±0.79 (serum). No significant (P>0.05) difference between CJD patients and controls was observed. Conclusions– The results indicated that the CSF and serum of CJD patients showed no higher endogenous levels of MDA as compared to normal healthy controls. These findings provide no evidence for an additional role of oxidative stress in the pathogenetic mechanism underlying CJD neurodegeneration."],["dc.identifier.doi","10.1034/j.1600-0404.2000.9s290a.x"],["dc.identifier.gro","3151697"],["dc.identifier.pmid","10987323"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8516"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.notes.submitter","chake"],["dc.relation.issn","0001-6314"],["dc.title","Creutzfeldt-Jakob disease and oxidative stress"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","257"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Fortschritte der Neurologie · Psychiatrie"],["dc.bibliographiccitation.lastpage","261"],["dc.bibliographiccitation.volume","68"],["dc.contributor.author","Kropp, Stefan"],["dc.contributor.author","Schlimme, J."],["dc.contributor.author","Bleich, Stefan"],["dc.contributor.author","Wiltfang, J."],["dc.contributor.author","Dietrich, D. E."],["dc.contributor.author","Emrich, H. M."],["dc.date.accessioned","2018-11-07T10:47:09Z"],["dc.date.available","2018-11-07T10:47:09Z"],["dc.date.issued","2000"],["dc.description.abstract","The dementia of the Alzheimer type (DAT) is a chronic neurodegenerative illness. It will continue to increase because of rising life expectancy in the industrialized countries. Apart from the physicians interest to treat, there is also an economically justified interest to reduce the disease progression in this group of patients. The main intention of the treating physicians is to keep their patients independent as long as possible. Up to now Alzheimer's disease can only be treated symptomatically. The verified diagnosis of DAT still depends on the neuropathological investigation of brain tissue. Therefore the clinical diagnosis of DAT during lifetime should be supported by chemical analysis of typical changes in the cerebrospinal fluid (CSF) at an early stage. Meanwhile, several therapeutics with proven effectiveness in clinical studies are certified for the symptomatic treatment of DAT. However, these therapeutics are still relatively expansive. Due to this fact the clinical diagnosis of DAT should be supported by clinical-chemical markers before the beginning of such a treatment. In this paper we present the diagnostic steps in dementia patients, who are examined in our departments. Patients suspicious of DAT always are asked for a spinal tap in addition to other diagnostic tools. In case of a typical clinical constellation, the exclusion of a primarily vascular dementia as well as the proof of decreased A beta(1-42) peptides and an increased tau protein in CSF we recommend the new drugs for DAT as meaningful and justified therapeutics to yield optimal treatment."],["dc.description.abstract","Die Demenz vom Alzheimer-Typ (DAT) ist eine chronische neurodegenerative Erkrankung, die bei steigender Lebenserwartung in den Industrieländern weiter zunehmen wird. Neben der medizinischen Behandlungsindikation besteht auch ein volkswirtschaftlich berechtigtes Interesse, die Krankheitsprogression bei den Betroffenen zu vermindern und die Selbständigkeit der Patienten möglichst lange zu erhalten. Bisher kann die Erkrankung nur symptomatisch behandelt werden. Die Diagnose der Alzheimer-Demenz kann mit letzter Sicherheit erst durch die neuropathologische Untersuchung von Hirngewebe gestellt werden. Um so wichtiger ist die Unterstützung der klinischen Verdachtsdiagnose durch den klinisch-chemischen Nachweis typischer Liquorveränderungen bei den Patienten. Mittlerweile sind mehrere Medikamente mit in klinischen Studien nachgewiesener Wirksamkeit für die symptomatische Behandlung der DAT zugelassen. Die Verschreibung dieser Therapeutika ist allerdings noch mit relativ hohen Kosten verbunden. Aufgrund dieser Tatsache sollte vor Beginn der Einstellung auf eines der neuen Antidementiva eine möglichst umfassende klinisch-chemische Diagnostik erfolgen. Wir stellen die diagnostischen Schritte bei Demenzkranken vor, die in unseren Abteilungen durchgeführt werden, wobei die Patienten bei Verdacht auf DAT und therapeutischer Option zur weiteren Abgrenzung des Krankheitsbildes liquorpunktiert werden. Bei typischer klinischer Symptomkonstellation, dem Ausschluss einer primär vaskulären Demenz sowie dem Nachweis erniedrigter Aβ1 - 42 und eines erhöhten Tau-Proteins im Liquor halten wir eine Behandlung mit neuen Antidementiva für therapeutisch sinnvoll und gerechtfertigt."],["dc.identifier.doi","10.1055/s-2000-11808"],["dc.identifier.isi","000087934000003"],["dc.identifier.pmid","10923250"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/47906"],["dc.language.iso","de"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0720-4299"],["dc.title","Diagnostische Schritte bei Alzheimer-Demenz vor Therapiebeginn mit neuen Antidementiva"],["dc.title.alternative","Diagnostic steps in Alzheimer dementia before treatment with new antidimentives"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]