Kamrowski-Kruck, Heike

[["dc.bibliographiccitation.firstpage","613"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Alzheimer s Disease"],["dc.bibliographiccitation.lastpage","622"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Klafki, Hans-Wolfgang"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Kamrowski-Kruck, Heike"],["dc.contributor.author","Maler, Juan Manuel"],["dc.contributor.author","Mueller, Katharina"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Heuser, Isabella"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Popp, Julius"],["dc.contributor.author","Froelich, Lutz"],["dc.contributor.author","Wolf, Stefanie"],["dc.contributor.author","Prinz, Berit"],["dc.contributor.author","Luckhaus, Christian"],["dc.contributor.author","Schroeder, Johannes"],["dc.contributor.author","Pantel, Johannes"],["dc.contributor.author","Gertz, Hermann-Josef"],["dc.contributor.author","Koelsch, Heike"],["dc.contributor.author","Mueller, Bernhard W."],["dc.contributor.author","Esselmann, Hermann"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, Jens"],["dc.date.accessioned","2018-11-07T08:34:46Z"],["dc.date.available","2018-11-07T08:34:46Z"],["dc.date.issued","2009"],["dc.description.abstract","The clinical diagnosis of neurodegenerative disorders can be supported by soluble biomarkers in cerebrospinal fluid (CSF), such as tau protein, phospho-tau, and amyloid-beta peptides. In particular, increased CSF levels of phospho-tau in Alzheimer's disease appear to reflect disease specific pathological processes. We report here evidence for the presence of soluble MAP-kinase ERK1/2 in a small set of human CSF samples from patients with Alzheimer's disease, frontotemporal degeneration, and mild cognitive impairment. The level of total ERK1/2 in CSF as measured by electrochemiluminescent assay was correlated with that of total tau and phospho-tau. A small fraction of ERK1/2 in a pooled CSF sample was found to be in the doubly phosphorylated (activated) state. Our findings suggest that i) MAP kinase ERK1/2 is apparently released under neurodegenerative conditions in parallel with tau and phospho-tau and ii) in the future, it might be possible to find in CSF samples evidence for disease related alterations in brain kinase signaling pathways by use of highly sensitive and activation-state specific anti-kinase antibodies."],["dc.identifier.doi","10.3233/JAD-2009-1167"],["dc.identifier.isi","000272860100013"],["dc.identifier.pmid","19625747"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17898"],["dc.notes.claim","Wed Nov 07 12:36:41 UTC 2018:dc_contributor_author:Hallo Sabine, das ist nicht mein Artikel.... :-)"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Ios Press"],["dc.relation.issn","1387-2877"],["dc.title","Measurement of ERK 1/2 in CSF from Patients with Neuropsychiatric Disorders and Evidence for the Presence of the Activated Form"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","18"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","26"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Hasselblatt, M."],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Loffler, B. M."],["dc.contributor.author","Kamrowski-Kruck, Heike"],["dc.contributor.author","von Ahsen, N."],["dc.contributor.author","Siren, A. L."],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2018-11-07T09:12:33Z"],["dc.date.available","2018-11-07T09:12:33Z"],["dc.date.issued","2001"],["dc.description.abstract","Astrocytes are known to possess an effective endothelin (ET) eliminatory system which involves astrocytic ETA and ETB receptors and may become particularly relevant under pathophysiological conditions. The present study has therefore been designed to explore the effect of standardized hypoxia on extracellular concentrations of endothelin-1 (ET-1) and on endothelin-converting enzyme (ECE) activity in primary rat astrocytes genetically (sl/sl) or experimentally (dexamethasone) deficient in ETB receptors. The results revealed (1) a hypoxia-mediated decrease of extracellular ET-1 in wildtype astrocytes (+/+) that was not observed in ETB-deficient (sl/sl) cultures; (2) an ET receptor antagonist-induced increase in ET-1 in the media of both genotypes with further elevation upon hypoxia in +/+ cultures only; (3) augmentation of the dexamethasone-induced increase in extracellular ET-1 by hypoxia in +/+, but not in sl/sl cultures; (4) synergistic reduction of ETB gene transcription by hypoxia and dexamethasone; and (5) significant increases in endothelin-converting enzyme activity in the presence of hypoxia. To conclude, hypoxia stimulates astrocytic release of mature ET-1, This stimulation is (over)compensated for by increased ET-1 binding to functional ETB receptors. ETB deficiency, whether genetic or experimentally induced, impairs elimination of extracellular (C) 2001 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/glia.1036"],["dc.identifier.isi","000167958400003"],["dc.identifier.pmid","11284016"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26960"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley"],["dc.relation.issn","1098-1136"],["dc.relation.issn","0894-1491"],["dc.title","Role of the astrocytic ETB receptor in the regulation of extracellular endothelin-1 during hypoxia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3485"],["dc.bibliographiccitation.issue","16"],["dc.bibliographiccitation.journal","Neuroreport"],["dc.bibliographiccitation.lastpage","3488"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Hasselblatt, M."],["dc.contributor.author","Kamrowski-Kruck, Heike"],["dc.contributor.author","Heyer, A."],["dc.contributor.author","Unzicker, C."],["dc.contributor.author","Siren, A. L."],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2018-11-07T11:00:45Z"],["dc.date.available","2018-11-07T11:00:45Z"],["dc.date.issued","2000"],["dc.description.abstract","The potential of erythropoietin (EPO) to reduce hypoxia-induced cell death has been investigated in 5-day-old primary cultures of rat postnatal hippocampal neurons. Application of EPO (100 pM) at the start of hypoxia resulted in a significant reduction of neuronal death (33.0 +/- 7.5% in cells incubated with EPO vs 56.75 +/- 7.3% in non-treated cells; n = 4, p < 0.021). Similiar results were obtained upon application of cycloheximide (CHX; 1 M) simultaneously with hypoxia (34.75 +/- 5.6% vs 56.75 +/- 7.3% with and without CHX, respectively, n = 4, p < 0.035), indicating that hypoxia-induced neuronal death is an active, protein synthesis-dependent process. Both, EPO and EPO receptor (EPOR) were found to; be expressed after hypoxia in hippocampal neurons in vitro and in vivo. These results demonstrate for the first time that EPO can reverse hypoxia-induced neuronal death when applied simultaneously with the hypoxic stimulus. NeuroReport 11:3485-3488 (C) 2000 Lippincott Williams & Wilkins."],["dc.identifier.doi","10.1097/00001756-200011090-00017"],["dc.identifier.isi","000165301600017"],["dc.identifier.pmid","11095504"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50997"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0959-4965"],["dc.title","Survival of hippocampal neurons in culture upon hypoxia: effect of erythropoietin"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","138"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.bibliographiccitation.lastpage","145"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Kamrowski-Kruck, Heike"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Heuser, Isabella"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Popp, J."],["dc.contributor.author","Buerger, Katharina"],["dc.contributor.author","Hampel, Harald"],["dc.contributor.author","Froelich, Lutz"],["dc.contributor.author","Wolf, S."],["dc.contributor.author","Prinz, Berit"],["dc.contributor.author","Jahn, Holger"],["dc.contributor.author","Luckhaus, C. H."],["dc.contributor.author","Perneczky, Robert"],["dc.contributor.author","Huell, Michael"],["dc.contributor.author","Schroeder, J."],["dc.contributor.author","Kessler, H."],["dc.contributor.author","Pantel, Johannes"],["dc.contributor.author","Gertz, H-J"],["dc.contributor.author","Klafki, H-W"],["dc.contributor.author","Koelsch, Heike"],["dc.contributor.author","Reulbach, Udo"],["dc.contributor.author","Esselmann, Herrmann"],["dc.contributor.author","Maler, Juan Manuel"],["dc.contributor.author","Bibl, Mirko"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Wiltfang, J."],["dc.date.accessioned","2018-11-07T08:46:25Z"],["dc.date.available","2018-11-07T08:46:25Z"],["dc.date.issued","2010"],["dc.description.abstract","In this report, we present the results of a multicenter study to test analytic and diagnostic performance of soluble forms of amyloid precursor proteins alpha and beta (sAPP alpha and sAPP beta) in the cerebrospinal fluid (CSF) of patients with different forms of dementing conditions. CSF samples were collected from 188 patients with early dementia (mini-mental state examination >= 20 in majority of cases) and mild cognitive impairment (MCI) in 12 gerontopsychiatric centers, and the clinical diagnoses were supported by neurochemical dementia diagnostic (NDD) tools: CSF amyloid beta peptides, Tau and phospho-Tau. sAPP alpha and sAPP beta were measured with multiplexing method based on electrochemiluminescence. sAPP alpha and sAPP beta CSF concentrations correlated with each other with very high correlation ratio (R= 0.96, P < 0.001). We observed highly significantly increased sAPP alpha and sAPP beta CSF concentrations in patients with NDD characteristic for Alzheimer's disease (AD) compared to those with NDD negative results. sAPP alpha and sAPP beta highly significantly separated patients with AD, whose diagnosis was supported by NDD findings (sAPP alpha: cutoff, 117.4 ng ml(-1), sensitivity, 68%, specificity, 85%, P< 0.001; sAPP beta: cutoff, 181.8 ng ml(-1), sensitivity, 75%, specificity, 85%, P < 0.001), from the patients clinically assessed as having other dementias and supported by NDD untypical for AD. We conclude sAPP alpha and sAPP beta might be regarded as novel promising biomarkers supporting the clinical diagnosis of AD. Molecular Psychiatry (2010) 15, 138-145; doi: 10.1038/mp.2008.84; published online 29 July 2008"],["dc.identifier.doi","10.1038/mp.2008.84"],["dc.identifier.isi","000273876000006"],["dc.identifier.pmid","18663368"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20687"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1359-4184"],["dc.title","Soluble amyloid precursor proteins in the cerebrospinal fluid as novel potential biomarkers of Alzheimer's disease: a multicenter study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]