Jacob, Sonja

[["dc.bibliographiccitation.firstpage","186"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Pineal Research"],["dc.bibliographiccitation.lastpage","187"],["dc.bibliographiccitation.volume","33"],["dc.contributor.author","Jacob, Sonja"],["dc.contributor.author","Poeggeler, Burkhard"],["dc.contributor.author","Weishaupt, Jochen H."],["dc.contributor.author","Sirén, Anna-Leena"],["dc.contributor.author","Hardeland, Rüdiger"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:45:41Z"],["dc.date.available","2017-09-07T11:45:41Z"],["dc.date.issued","2002"],["dc.identifier.doi","10.1034/j.1600-079X.2002.02943.x"],["dc.identifier.gro","3150431"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7194"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","0742-3098"],["dc.title","Melatonin as a candidate compound for neuroprotection in amyotrophic lateral sclerosis (ALS): high tolerability of daily oral melatonin administration in ALS patients"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","598"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Neuroradiology"],["dc.bibliographiccitation.lastpage","600"],["dc.contributor.author","Jacob, Sonja"],["dc.contributor.author","Finsterbusch, J."],["dc.contributor.author","Weishaupt, Jochen H."],["dc.contributor.author","Khorram-Sefat, D."],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:45:43Z"],["dc.date.available","2017-09-07T11:45:43Z"],["dc.date.issued","2003"],["dc.description.abstract","Amyotrophic lateral sclerosis (ALS) is a predominantly clinical and electromyographic diagnosis. Conventional MRI reveals atrophy of the motor system, particularly the pyramidal tract, in the advanced stages but does not provide a sensitive measure of disease progression. Three patients with different principal symptoms of ALS, i.e., with predominant involvement of the upper (UMN) or lower (UMN) motor neurons, or bulbar disease, respectively, underwent serial clinical examination including lung function tests, conventional MRI, and diffusion tensor imaging (DTI). MRI demonstrated changes in of the pyramidal tract without measurable variation on follow-up. The patient with UMN involvement showed remarkable progressive loss of diffusion anisotropy in the pyramidal tract. DTI might be useful, together with clinical follow-up, as an objective morphological marker in therapeutic trials."],["dc.identifier.doi","10.1007/s00234-003-1014-0"],["dc.identifier.gro","3150437"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7201"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.relation.issn","0028-3940"],["dc.title","Diffusion tensor imaging for long-term follow-up of corticospinal tract degeneration in amyotrophic lateral sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["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"]]

[["dc.bibliographiccitation.firstpage","195"],["dc.bibliographiccitation.issue","3-4"],["dc.bibliographiccitation.journal","Metabolic Brain Disease"],["dc.bibliographiccitation.lastpage","206"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Aust, Carlotta"],["dc.contributor.author","Krampe, Henning"],["dc.contributor.author","Jahn, Henriette"],["dc.contributor.author","Jacob, Sonja"],["dc.contributor.author","Herrmann, Manfred"],["dc.contributor.author","Sirén, Anna-Leena"],["dc.date.accessioned","2017-09-07T11:46:24Z"],["dc.date.available","2017-09-07T11:46:24Z"],["dc.date.issued","2004"],["dc.description.abstract","With the increased life expectancy in western industrialized countries, the incidence and prevalence of brain diseases dramatically increased. Stroke and a wide spectrum of neuropsychiatric illnesses such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, traumatic head injury, and schizophrenia all lead to severe disability. However, targeted effective therapies for treatment of these diseases are lacking. Even more frustrating is the fact that we do not yet clearly understand the basic mechanisms underlying the disease processes in these conditions. We propose a hypothesis of loss of neuronal function via a final common deleterious pathway in this clinically very heterogeneous disease group. This review presents a novel neuroprotective concept for treatment of brain disease: Erythropoietin (EPO). EPO is a natural body-own-protein hormone that has been used for treatment of anemia for more than a decade. The neuroprotective approach using EPO in brain disease represents a totally new frontier. The “Göttingen EPO-stroke trial” represents the first effective use in man of a neuroprotective therapy in an acute brain disease while the experimental EPO therapy to combat cognitive decline in patients with schizophrenia will be introduced as an example of a neuroprotective strategy for a chronic brain disease."],["dc.identifier.gro","3150507"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7279"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","0885-7490"],["dc.subject","EPO; stroke; schizophrenia; treatment; regeneration."],["dc.title","Erythropoietin: Novel approaches to neuroprotection in human brain disease"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","4121"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Anticancer Research"],["dc.bibliographiccitation.lastpage","4125"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Strik, Herwig M."],["dc.contributor.author","Spreer, Annette"],["dc.contributor.author","Nagel, Holger"],["dc.contributor.author","Jacob, Sonja"],["dc.contributor.author","Jung, Wolfram"],["dc.contributor.author","Kitze, Bernd"],["dc.contributor.author","Bähr, Mathias"],["dc.date.accessioned","2017-09-07T11:43:10Z"],["dc.date.available","2017-09-07T11:43:10Z"],["dc.date.issued","2004"],["dc.description.abstract","A 69-year-old female patient was treated for primary CNS-lymphoma (PCNSL) starting from August 2002. As her general condition allowed no high-dose methotrexate (MTX) therapy, radiotherapy was administered as a first-line treatment. CSF involvement could be managed by intrathecal Ara-C. Her general condition and cognitive status stabilized., but did not improve for 3 months. Therefore, oral chemotherapy with Temozolomide 200mg/m(2) was initiated. After two courses, which were tolerated without any problems, the patient's Karnofsky performance index had improved from 40% to 50%, the Mini-Mental Status rose from 16 to 27130. The CSF-cell count was elevated again to 23 cells/mul without signs of meningeal relapse. Unfortunately, the patient died unexpectedly front suspected pulmonary embolism. We conclude that adjuvant Temozolomide chemotherapy can improve the general condition and cognition in patients with PCNSL even when the general condition is poor. Long-term effects and neurotoxicity remain to be analysed in prospective trials, as well as the efficacy in leptomeningeal disease."],["dc.identifier.gro","3143931"],["dc.identifier.isi","000227014500066"],["dc.identifier.pmid","15736462"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1499"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0250-7005"],["dc.title","Clinical Response Following Adjuvant Temozolomide in a Patient with Primary Cerebral Lymphoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["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"]]

[["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"]]