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Knerlich, Friederike
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Knerlich, Friederike
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Knerlich, Friederike
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Knerlich, F.
Knerlich-Lukoschus, Friederike
Knerlich-Lukoschus, F.
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2005Journal Article [["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Journal of Neurology Neurosurgery & Psychiatry"],["dc.bibliographiccitation.volume","76"],["dc.contributor.author","Knerlich, F."],["dc.contributor.author","Verheggen, Raphaela"],["dc.date.accessioned","2018-11-07T10:55:27Z"],["dc.date.available","2018-11-07T10:55:27Z"],["dc.date.issued","2005"],["dc.format.extent","1359"],["dc.identifier.doi","10.1136/jnnp.2004.061127"],["dc.identifier.isi","000231960700009"],["dc.identifier.pmid","16170076"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/49787"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","B M J Publishing Group"],["dc.relation.issn","0022-3050"],["dc.title","Feeding cats might be dangerous: penetrating orbital and brain injury without neurological deficits"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2004Journal Article [["dc.bibliographiccitation.firstpage","42"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.bibliographiccitation.lastpage","54"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Degner, D."],["dc.contributor.author","Meller, Johannes"],["dc.contributor.author","Brines, Michael"],["dc.contributor.author","Behe, M."],["dc.contributor.author","Hasselblatt, Martin"],["dc.contributor.author","Woldt, Helge"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Knerlich, Friederike"],["dc.contributor.author","Jacob, Silke"],["dc.contributor.author","von Ahsen, Nicolas"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Brück, W."],["dc.contributor.author","Rüther, Eckart"],["dc.contributor.author","Cerami, A."],["dc.contributor.author","Becker, Wolfgang"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.date.accessioned","2017-09-07T11:46:26Z"],["dc.date.available","2017-09-07T11:46:26Z"],["dc.date.issued","2004"],["dc.description.abstract","Erythropoietin (EPO) is a candidate compound for neuroprotection in human brain disease capable of combating a spectrum of pathophysiological processes operational during the progression of schizophrenic psychosis. The purpose of the present study was to prepare the ground for its application in a first neuroprotective add-on strategy in schizophrenia, aiming at improvement of cognitive brain function as well as prevention/slowing of degenerative processes. Using rodent studies, primary hippocampal neurons in culture, immunohistochemical analysis of human post-mortem brain tissue and nuclear imaging technology in man, we demonstrate that: (1) peripherally applied recombinant human (rh) EPO penetrates into the brain efficiently both in rat and humans, (2) rhEPO is enriched intracranially in healthy men and more distinctly in schizophrenic patients, (3) EPO receptors are densely expressed in hippocampus and cortex of schizophrenic subjects but distinctly less in controls, (4) rhEPO attenuates the haloperidol-induced neuronal death in vitro, and (4) peripherally administered rhEPO enhances cognitive functioning in mice in the context of an aversion task involving cortical and subcortical pathways presumably affected in schizophrenia. These observations, together with the known safety of rhEPO, render it an interesting compound for neuroprotective add-on strategies in schizophrenia and other human diseases characterized by a progressive decline in cognitive performance."],["dc.identifier.doi","10.1038/sj.mp.4001442"],["dc.identifier.gro","3150503"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7274"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.relation.issn","1359-4184"],["dc.subject","recombinant human erythropoietin; EPO; schizophrenia; clinical; rodent; SPECT"],["dc.title","Erythropoietin: a candidate compound for neuroprotection in schizophrenia"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]Details DOI2005Journal Article [["dc.bibliographiccitation.firstpage","862"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Proceedings of the National Academy of Sciences of the United States of America"],["dc.bibliographiccitation.lastpage","867"],["dc.bibliographiccitation.volume","102"],["dc.contributor.author","Hasselblatt, Martin"],["dc.contributor.author","Knerlich, Friederike"],["dc.contributor.author","von Ahsen, N."],["dc.contributor.author","Jacob, Sonja"],["dc.contributor.author","Sperling, S."],["dc.contributor.author","Woldt, H."],["dc.contributor.author","Vehmeyer, K."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Sirén, A.-L."],["dc.contributor.author","Ehrenreich, H."],["dc.date.accessioned","2017-09-07T11:46:36Z"],["dc.date.available","2017-09-07T11:46:36Z"],["dc.date.issued","2005"],["dc.description.abstract","Central nervous and hematopoietic systems share developmental features. We report that thrombopoietin (TPO), a stimulator of platelet formation, acts in the brain as a counterpart of erythropoietin (EPO), a hematopoietic growth factor with neuroprotective properties. TPO is most prominent in postnatal brain, whereas EPO is abundant in embryonic brain and decreases postnatally. Upon hypoxia, EPO and its receptor are rapidly reexpressed, whereas neuronal TPO and its receptor are down-regulated. Unexpectedly, TPO is strongly proapoptotic in the brain, causing death of newly generated neurons through the Ras-extracellular signal-regulated kinase 1/2 pathway. This effect is not only inhibited by EPO but also by neurotrophins. We suggest that the proapoptotic function of TPO helps to select for neurons that have acquired target-derived neurotrophic support."],["dc.identifier.doi","10.1073/pnas.0406008102"],["dc.identifier.gro","3150545"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7318"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.relation.issn","0027-8424"],["dc.subject","astrocytes; erythropoietin; neurons; differentiation; development"],["dc.title","A hematopoietic growth factor, thrombopoietin, has a proapoptotic role in the brain"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]Details DOI2002Conference Abstract [["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Stroke"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Hasselblatt, M."],["dc.contributor.author","Piotr, L."],["dc.contributor.author","Dembowski, C."],["dc.contributor.author","Cepek, L."],["dc.contributor.author","Stiefel, M."],["dc.contributor.author","Rustenbeck, Hans Heino"],["dc.contributor.author","Jacob, S."],["dc.contributor.author","Knerlich, F."],["dc.contributor.author","Gleiter, Christoph H."],["dc.contributor.author","Prange, Hilmar"],["dc.contributor.author","Siren, A. L."],["dc.date.accessioned","2018-11-07T10:33:49Z"],["dc.date.available","2018-11-07T10:33:49Z"],["dc.date.issued","2002"],["dc.format.extent","354"],["dc.identifier.isi","000173147700143"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44705"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.issn","0039-2499"],["dc.title","Erythropoietin treatment for acute stroke: A randomized double-blind proof-of concept trial in man"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details WOS2001Journal Article [["dc.bibliographiccitation.firstpage","271"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","276"],["dc.bibliographiccitation.volume","101"],["dc.contributor.author","Siren, A. L."],["dc.contributor.author","Knerlich, F."],["dc.contributor.author","Poser, Wolfgang"],["dc.contributor.author","Gleiter, Christoph H."],["dc.contributor.author","Bruck, Wolfgang W."],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2018-11-07T09:17:30Z"],["dc.date.available","2018-11-07T09:17:30Z"],["dc.date.issued","2001"],["dc.description.abstract","Using immunohistochemistry, expression of erythropoietin (EPO), a hypoxia-inducible neuroprotective factor, and its receptor (EPOR) were investigated in human brain tissue after ischemia/hypoxia. Autopsy brains of neuropathologically normal subjects were compared to those with ischemic infarcts or hypoxic damage. In normal brain, weak EPO/EPOR immunoreactivity was mainly neuronal. In fresh infarcts, EPO immunoreactivity appeared in vascular endothelium, EPOR in microvessels and neuronal fibers. In older infarcts reactive astrocytes exhibited EPO/EPOR immunoreactivity. Acute hypoxic brain damage was associated with vascular EPO expression, older hypoxic damage with EPO/EPOR immunoreactivity in reactive astrocytes. The pronounced up-regulation of EPO/EPOR in human ischemic/hypoxic brains underlines their role as an endogenous neuroprotective system and suggests a novel therapeutic potential in cerebrovascular disease for EPO, a clinically well-characterized and safe compound."],["dc.identifier.isi","000167526200013"],["dc.identifier.pmid","11307627"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28185"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0001-6322"],["dc.title","Erythropoietin and erythropoietin receptor in human ischemic/hypoxic brain"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details PMID PMC WOS2021Journal Article [["dc.bibliographiccitation.firstpage","3376"],["dc.bibliographiccitation.issue","24"],["dc.bibliographiccitation.journal","Journal of Neurotrauma"],["dc.bibliographiccitation.lastpage","3392"],["dc.bibliographiccitation.volume","38"],["dc.contributor.author","Cohrs, Gesa"],["dc.contributor.author","Blumenröther, Ann-Kathrin"],["dc.contributor.author","Sürie, Jan-Philip"],["dc.contributor.author","Synowitz, Michael"],["dc.contributor.author","Held-Feindt, Janka"],["dc.contributor.author","Knerlich-Lukoschus, Friederike"],["dc.date.accessioned","2022-01-11T14:05:53Z"],["dc.date.available","2022-01-11T14:05:53Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1089/neu.2021.0091"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/97769"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-507"],["dc.relation.eissn","1557-9042"],["dc.relation.issn","0897-7151"],["dc.rights.uri","https://www.liebertpub.com/nv/resources-tools/text-and-data-mining-policy/121/"],["dc.title","Fetal and Perinatal Expression Profiles of Proinflammatory Cytokines in the Neuroplacodes of Rats with Myelomeningoceles: A Contribution to the Understanding of Secondary Spinal Cord Injury in Open Spinal Dysraphism"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2002Journal Article Research Paper [["dc.bibliographiccitation.firstpage","495"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Molecular Medicine"],["dc.bibliographiccitation.lastpage","505"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Hasselblatt, Martin"],["dc.contributor.author","Dembowski, Christoph"],["dc.contributor.author","Cepek, Lukas"],["dc.contributor.author","Lewczuk, Pjotr"],["dc.contributor.author","Stiefel, Michael"],["dc.contributor.author","Rustenbeck, Hans-Heino"],["dc.contributor.author","Breiter, Norbert"],["dc.contributor.author","Jacob, Sonja"],["dc.contributor.author","Knerlich, Friederike"],["dc.contributor.author","Bohn, Matthias"],["dc.contributor.author","Poser, Wolfgang"],["dc.contributor.author","Rüther, Eckart"],["dc.contributor.author","Kochen, Michael"],["dc.contributor.author","Gefeller, Olaf"],["dc.contributor.author","Gleiter, Christoph H."],["dc.contributor.author","Wessel, Thomas C."],["dc.contributor.author","Ryck, Marc de"],["dc.contributor.author","Itri, Loretta"],["dc.contributor.author","Prange, Hilmar"],["dc.contributor.author","Cerami, Anthony"],["dc.contributor.author","Brines, Michael"],["dc.contributor.author","Siren, Anna-Leena"],["dc.date.accessioned","2017-09-07T11:45:41Z"],["dc.date.available","2017-09-07T11:45:41Z"],["dc.date.issued","2002"],["dc.description.abstract","Background: Erythropoietin (EPO) and its receptor play a major role in embryonic brain, are weakly expressed in normal postnatal/adult brain and up-regulated upon metabolic stress. EPO protects neurons from hypoxic/ ischemic injury. The objective of this trial is to study the safety and efficacy of recombinant human EPO (rhEPO) for treatment of ischemic stroke in man. Materials and Methods: The trial consisted of a safety part and an efficacy part. in the safety study, 13 patients received rhEPO intravenously (3.3 x 10(4) IU/50 m/130 min) once daily for the first 3 days after stroke. in the double-blind randomized proof-of-concept trial, 40 patients received either rhEPO or saline. Inclusion criteria were age {.extbackslash}textless80 years, ischemic stroke within the middle cerebral artery territory confirmed by diffusion-weighted MRI, symptom onset {.extbackslash}textless8 hr before drug administration, and deficits on stroke scales. The study endpoints were functional outcome at day 30 (Barthel index, modified Rankin scale), NIH and Scandinavian stroke scales, evolution of infarct size (sequential MRI evaluation using diffusion-weighted [DWI] and fluid-attenuated inversion recovery sequences [FLAIR]) and the damage marker S100ss. Results: No safety concerns were identified. Cerebrospinal fluid EPO increased to 60-100 times that of nontreated patients, proving that intravenously administered rhEPO reaches the brain. in the efficacy trial, patients received rhEPO within 5 hr of onset of symptoms (median, range 2:40-7:55). Admission neurologic scores and serum S100beta concentrations were strong predictors of outcome. Analysis of covariance controlled for these two variables indicated that rhEPO treatment was associated with an improvement in follow-up and outcome scales. A strong trend for reduction in infarct size in rhEPO patients as compared to controls was observed by MRI. Conclusion: intravenous high-dose rhEPO is well tolerated in acute ischemic stroke and associated with an improvement in clinical outcome at 1 month. A larger scale clinical trial is warranted."],["dc.identifier.gro","3150429"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7192"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","1076-1551"],["dc.relation.orgunit","Institut für Allgemeinmedizin"],["dc.title","Erythropoietin therapy for acute stroke is both safe and beneficial"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","no"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]Details2004Journal Article [["dc.bibliographiccitation.firstpage","503"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","ANATOMY AND EMBRYOLOGY"],["dc.bibliographiccitation.lastpage","512"],["dc.bibliographiccitation.volume","207"],["dc.contributor.author","Knabe, Wolfgang"],["dc.contributor.author","Knerlich, F."],["dc.contributor.author","Washausen, Stefan"],["dc.contributor.author","Kietzmann, Thomas"],["dc.contributor.author","Siren, A. L."],["dc.contributor.author","Brunnett, G."],["dc.contributor.author","Kuhn, H. J."],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2018-11-07T10:50:26Z"],["dc.date.available","2018-11-07T10:50:26Z"],["dc.date.issued","2004"],["dc.description.abstract","The expression patterns of erythropoietin (EPO) and its receptor (EPOR) were investigated in the midbrain and in adjacent parts of the synencephalon and hindbrain of embryonic C57Bl mice. On embryonic (E) day 8 (E8), virtually all neuroepithelial cells expressed EPOR. After neural tube closure, subsets of these cells downregulated EPOR. In contrast, radial glial cells were EPOR-immunolabeled from E11 onwards. Simultaneously, subpopulations of early developing neurons upregulated EPO and expressed HIF-1, known to transcriptionally activate EPO. Three-dimensional reconstructions revealed subpopulations of EPO-expressing neurons: (1) in the trigeminal mesencephalic nucleus (TMN), (2) at the rostral transition of the midbrain and synencephalon, (3) in the basal plate of the midbrain, (4) in the trigeminal motor nucleus, and (5) in the trigeminal principal sensory nucleus. In the rostral midbrain and synencephalon, EPO-immunoreactive neurons were attached to EPOR-expressing radial glial cells. The identity of radial glial cells was proven by their immunoreactivity for antibodies against astrocyte-specific glutamate transporter, brain lipid-binding protein, and nestin. From E12.5 onwards EPOR was downregulated in radial glial cells. Viable neurons of the TMN continued to express EPO and upregulated EPOR. Our findings provide new evidence that components of the EPO system are present in distinct locations of the embryonic brain and, by interactions between neurons and radial glial cells as well as among clustered TMN neurons, may contribute to its morphogenesis. Whether the observed expression patterns of EPO and EPOR may reflect EPO-mediated trophic and/or antiapoptotic effects on neurons is discussed."],["dc.identifier.doi","10.1007/s00429-003-0365-y"],["dc.identifier.isi","000220086500009"],["dc.identifier.pmid","14770308"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/48650"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0340-2061"],["dc.title","Expression patterns of erythropoietin and its receptor in the developing midbrain"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2022Journal Article [["dc.bibliographiccitation.journal","Neurosurgical Review"],["dc.contributor.author","Jünger, Stephanie T."],["dc.contributor.author","Knerlich-Lukoschus, Friederike"],["dc.contributor.author","Röhrig, Andreas"],["dc.contributor.author","Al Hourani, Jasmin"],["dc.contributor.author","Kunze, Sandra"],["dc.contributor.author","Eberle, Julia"],["dc.contributor.author","Oelkers, Peter"],["dc.contributor.author","Messing-Jünger, Martina"],["dc.date.accessioned","2022-07-01T07:35:36Z"],["dc.date.available","2022-07-01T07:35:36Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1007/s10143-022-01809-0"],["dc.identifier.pii","1809"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112215"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-581"],["dc.relation.eissn","1437-2320"],["dc.rights.uri","https://www.springer.com/tdm"],["dc.title","Clinical variety and prognosis of intracranial arachnoid cysts in children"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]Details DOI2002Journal Article [["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Molecular Medicine"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Ehrenreich, H."],["dc.contributor.author","Hasselblatt, M."],["dc.contributor.author","Cepek, L."],["dc.contributor.author","Jacob, Sonja"],["dc.contributor.author","Knerlich, F."],["dc.contributor.author","Sirén, A.-L."],["dc.date.accessioned","2017-09-07T11:45:47Z"],["dc.date.available","2017-09-07T11:45:47Z"],["dc.date.issued","2002"],["dc.description.abstract","BACKGROUND: Erythropoietin (EPO) and its receptor play a major role in embryonic brain, are weakly expressed in normal postnatal/adult brain and up-regulated upon metabolic stress. EPO protects neurons from hypoxic/ ischemic injury. The objective of this trial is to study the safety and efficacy of recombinant human EPO (rhEPO) for treatment of ischemic stroke in man. MATERIALS AND METHODS: The trial consisted of a safety part and an efficacy part. In the safety study, 13 patients received rhEPO intravenously (3.3 X 10(4) IU/50 ml/30 min) once daily for the first 3 days after stroke. In the double-blind randomized proof-of-concept trial, 40 patients received either rhEPO or saline. Inclusion criteria were age <80 years, ischemic stroke within the middle cerebral artery territory confirmed by diffusion-weighted MRI, symptom onset <8 hr before drug administration, and deficits on stroke scales. The study endpoints were functional outcome at day 30 (Barthel Index, modified Rankin scale), NIH and Scandinavian stroke scales, evolution of infarct size (sequential MRI evaluation using diffusion-weighted [DWI] and fluid-attenuated inversion recovery sequences [FLAIR]) and the damage marker S100ss. RESULTS: No safety concerns were identified. Cerebrospinal fluid EPO increased to 60-100 times that of nontreated patients, proving that intravenously administered rhEPO reaches the brain. In the efficacy trial, patients received rhEPO within 5 hr of onset of symptoms (median, range 2:40-7:55). Admission neurologic scores and serum S100beta concentrations were strong predictors ofoutcome. Analysis of covariance controlled for these two variables indicated that rhEPO treatment was associated with an improvement in follow-up and outcome scales. A strong trend for reduction in infarct size in rhEPO patients as compared to controls was observed by MRI. CONCLUSION: Intravenous high-dose rhEPO is well tolerated in acute ischemic stroke and associated with an improvement in clinical outcome at 1 month. A larger scale clinical trial is warranted."],["dc.identifier.gro","3150458"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7224"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","chake"],["dc.title","Erytropoietin treatment for human stroke is safe and beneficial"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]Details