Schulz, Jörg Bernhard

[["dc.bibliographiccitation.firstpage","49"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","50"],["dc.bibliographiccitation.volume","110"],["dc.contributor.author","Drinkut, Anja"],["dc.contributor.author","Nagel, F."],["dc.contributor.author","Kramer, Edgar R."],["dc.contributor.author","Kuegler, Sebastian"],["dc.contributor.author","Schulz, Joerg B."],["dc.date.accessioned","2018-11-07T08:28:17Z"],["dc.date.available","2018-11-07T08:28:17Z"],["dc.date.issued","2009"],["dc.identifier.isi","000266400900131"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16385"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell Publishing, Inc"],["dc.publisher.place","Malden"],["dc.relation.conference","4th European-Society-for-Neurochemistry Conference on Advances in Molecular Mechanisms of Neurological Disorders"],["dc.relation.eventlocation","Leipzig, GERMANY"],["dc.relation.issn","0022-3042"],["dc.title","Role of the RET/GDNF signaling pathway in protection of the nigro-striatal system in a MPTP mouse model for Parkinson's disease"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","204"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","The Cerebellum"],["dc.bibliographiccitation.lastpage","214"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Doehlinger, Susanne"],["dc.contributor.author","Hauser, Till-Karsten"],["dc.contributor.author","Borkert, Johannes"],["dc.contributor.author","Luft, Andreas R."],["dc.contributor.author","Schulz, Joerg B."],["dc.date.accessioned","2018-11-07T11:14:15Z"],["dc.date.available","2018-11-07T11:14:15Z"],["dc.date.issued","2008"],["dc.description.abstract","Magnetic resonance (MR) imaging is widely used to visualize atrophic processes that occur during the pathogenesis of spinocerebellar ataxias (SCAs). T1-weighted images are utilized to rate the atrophy of cerebellar vermis, cerebellar hemispheres, pons and midbrain. Signal changes in the basal ganglia and ponto-cerebellar fibers are evaluated by T2-weighted and proton density-weighted images. However, two-dimensional (2D) images do not allow a reliable quantification of the degree of atrophy. The latter is now possible through the application of three-dimensional (3D) true volumetric methods, which should be used for research purposes. Ideally, these methods should allow automated segmentation of contrast-defined boundaries by using region growing algorithms, which can be applied successfully in structures of the posterior fossa and basal ganglia. Thin slice thickness helps to minimize partial volume effects. Whereas volumetric approaches rely on predetermined anatomical boundaries, voxel-based morphometry has been developed to determine group differences between different types of SCA (cross-sectional studies) or within one SCA entity (longitudinal studies). We will review recent results and how these methods are currently used to (i) separate sporadic and dominantly inherited forms of cerebellar ataxias; (ii) identify specific SCA genotypes; (iii) correlate patho-anatomical changes with SCA disease symptoms or severity; and (iv) visualize and estimate the rate of progression in SCA."],["dc.identifier.doi","10.1007/s12311-008-0025-0"],["dc.identifier.isi","000259277100015"],["dc.identifier.pmid","18418677"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54087"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1473-4222"],["dc.title","Magnetic resonance imaging in spinocerebellar ataxias"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1674"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Movement Disorders"],["dc.bibliographiccitation.lastpage","1681"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Hauser, Till-Karsten"],["dc.contributor.author","Luft, Andreas R."],["dc.contributor.author","Skalej, Martin"],["dc.contributor.author","Naegele, Thomas"],["dc.contributor.author","Kircher, Tilo T. J."],["dc.contributor.author","Leube, Dirk T."],["dc.contributor.author","Schulz, Joerg B."],["dc.date.accessioned","2018-11-07T10:38:46Z"],["dc.date.available","2018-11-07T10:38:46Z"],["dc.date.issued","2006"],["dc.description.abstract","To visualize and quantify disease progression in multiple system atrophy (MSA) from cerebellar type (MSA-C), we combined two magnetic resonance imaging (MRI) techniques, voxel-based morphometry (VBM) and 3D-based volumetry. Patients suffering from MSA-C (n = 14) were imaged twice with an interval of 2.0 +/- 0.2 years. We first applied VBM to map brain morphology changes between MSA patients and controls and to identify brain areas that showed a significant amount of atrophy. Using 3D-based volumetry, we confirmed that in MSA-C patients, the brainstem including medulla and pons, vermis and cerebellar hemispheres, caudate nucleus and putamen showed significant atrophy compared with controls. Next, we used 3D-based volumetry to analyze the atrophy rates. Atrophy rates in patients with MSA were significantly different from controls for putamen (- 11.4% +/- 2.6%/year), vermis (-12.3% +/- 2.9%/year), and cerebellar hemispheres (-6.6% +/- 1.1%/year). The results show that 3D-based MRI volumetry is a tool that allows the disease progression of MSA to be followed over a time period of 2 years and suggest that it may serve as a surrogate marker in clinical trials to measure disease progression. (C) 2006 Movement Disorder Society."],["dc.identifier.doi","10.1002/mds.21032"],["dc.identifier.isi","000241745300016"],["dc.identifier.pmid","16830312"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45890"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","0885-3185"],["dc.title","Visualization and quantification of disease progression in multiple system atrophy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","123"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neurobiology of Disease"],["dc.bibliographiccitation.lastpage","133"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Straten, G"],["dc.contributor.author","Schmeer, C."],["dc.contributor.author","Kretz, A."],["dc.contributor.author","Gerhardt, Ellen"],["dc.contributor.author","Kugler, S."],["dc.contributor.author","Schulz, Joerg B."],["dc.contributor.author","Gravel, C."],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Isenmann, Stefan"],["dc.date.accessioned","2017-09-07T11:45:15Z"],["dc.date.available","2017-09-07T11:45:15Z"],["dc.date.issued","2002"],["dc.description.abstract","Following transection of the optic nerve (ON) in the adult rat, retinal ganglion cells (RGCs) undergo degeneration, and within 14 days 85% of axotomized RGCs die by apoptosis. Adenoviral delivery of the mammalian caspase inhibitor X-chromosome-linked inhibitor of apoptosis (Ad.XIAP) to the ON stump leads to expression exclusively in RGCs and rescues 18.9% of the RGCs that would degenerate without treatment. Following adenoviral vector injection into the vitreous body, bioactive glial cell line-derived neurotrophic factor (Ad.GDNF) is expressed in the retina and secreted to rescue 22.8% of lesioned RGCs. Here we report that coadministration of Ad.XIAP retrogradely directed to RGCs and intravitreal Ad.GDNF acts synergistically to protect axotomized RGCs. Combination treatment rescued 47.3% of RGCs that would undergo apoptosis without any treatment as opposed to 37.4% that would be expected if the two treatments acted independently. While without treatment only 15% of axotomized RGCs would survive, combination treatment resulted in survival of 55.4% of the total RGC population. These findings underline the neuroprotective potential of synergistic effects of a combination of different treatment strategies. (C) 2002 Elsevier Science (USA)."],["dc.identifier.doi","10.1006/nbdi.2002.0543"],["dc.identifier.gro","3144173"],["dc.identifier.isi","000179314100011"],["dc.identifier.pmid","12460552"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1768"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0969-9961"],["dc.title","Potential synergistic protection of retinal ganglion cells from axotomy-induced apoptosis by adenoviral administration of glial cell line-derived neurotrophic factor and X-chromosome-linked inhibitor of apoptosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","68"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neuroscience Letters"],["dc.bibliographiccitation.lastpage","71"],["dc.bibliographiccitation.volume","440"],["dc.contributor.author","Koelsch, Heike"],["dc.contributor.author","Jessen, Frank"],["dc.contributor.author","Wiltfang, Jens"],["dc.contributor.author","Lewczuk, Piotr"],["dc.contributor.author","Dichgans, Martin"],["dc.contributor.author","Kornhuber, Johannes"],["dc.contributor.author","Froelich, Lutz"],["dc.contributor.author","Heuser, Isabella"],["dc.contributor.author","Peters, Oliver"],["dc.contributor.author","Schulz, Joerg B."],["dc.contributor.author","Schwab, Sibylle G."],["dc.contributor.author","Maier, Wolfgang"],["dc.date.accessioned","2018-11-07T11:12:54Z"],["dc.date.available","2018-11-07T11:12:54Z"],["dc.date.issued","2008"],["dc.description.abstract","SORL1 gene variants were described as risk factors of Alzheimer's disease (AD). We investigated the association of four SORL1 variants with CSF levels of A beta(42) and A beta(40) in 153 AD patients recruited from a multicenter study of the German Competence Net Dementias. Only one SORL1 SNP was associated with altered A beta(42) levels in the single marker analysis (SNP21: p = 0.011), the other SNPs did not show an association with A beta(42) orA beta(40) CSF levels. Haplotype analysis identified a three marker SORL1 haplotype consisting of SNP19 T-allele, SNP21 G-allele and SNP23 A-allele (T/G/A) which was associated with reduced A beta(42) CSF levels in AD patients (p = 0.003). A beta(40) levels were also lower in carriers of this haplotype; however, this did not reach statistical significance (p = 0.15). We found a SORL1 haplotype which was associated with CSF levels of amyloid-P cleavage products, measured as altered levels of A beta(42). Thus our data suggest that: SORL1 gene variants might influence AD pathology. (C) 2008 Elsevier Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.neulet.2008.05.049"],["dc.identifier.isi","000257640200016"],["dc.identifier.pmid","18541377"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53768"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Ireland Ltd"],["dc.relation.issn","0304-3940"],["dc.title","Influence of SORL1 gene variants: Association with CSF amyloid-beta products in probable Alzheimer's disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neuropathology and Experimental Neurology"],["dc.bibliographiccitation.lastpage","13"],["dc.bibliographiccitation.volume","73"],["dc.contributor.author","Tauber, Simone C."],["dc.contributor.author","Harms, Kristian"],["dc.contributor.author","Falkenburger, Bjoern H."],["dc.contributor.author","Weis, Joachim"],["dc.contributor.author","Sellhaus, Bernd"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Schulz, Joerg B."],["dc.contributor.author","Reich, Arno"],["dc.date.accessioned","2018-11-07T09:46:12Z"],["dc.date.available","2018-11-07T09:46:12Z"],["dc.date.issued","2014"],["dc.description.abstract","Fas-apoptotic inhibitory molecule 2 (Faim2) is a neuron-specific membrane protein and a member of the evolutionary conserved lifeguard apoptosis regulatory gene family. Its neuroprotective effect in acute neurological diseases has been demonstrated in an in vivo model of focal cerebral ischemia. Here we show that Faim2 is physiologically expressed in the human brain with a changing pattern in cases of infectious meningoencephalitis.In Faim2-deficient mice, there was increased caspase-associated hippocampal apoptotic cell death and an increased extracellular signal-regulated kinase pattern during acute bacterial meningitis induced by subarachnoid infection with Streptococcus pneumoniae type 3 strain. However, after rescuing the animals by antibiotic treatment, Faim2 deficiency led to increased hippocampal neurogenesis at 7 weeks after infection. This was associated with improved performance of Faim2-deficient mice compared to wild-type littermates in the Morris water maze, a paradigm for hippocampal spatial learning and memory. Thus, Faim2 deficiency aggravated degenerative processes in the acute phase but induced regenerative processes in the repair phase of a mouse model of pneumococcal meningitis. Hence, time-dependent modulation of neuroplasticity by Faim2 may offer a new therapeutic approach for reducing hippocampal neuronal cell death and improving cognitive deficits after bacterial meningitis."],["dc.identifier.doi","10.1097/NEN.0000000000000020"],["dc.identifier.isi","000335647400001"],["dc.identifier.pmid","24335530"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/34817"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0022-3069"],["dc.title","Modulation of Hippocampal Neuroplasticity by Fas/CD95 Regulatory Protein 2 (Faim2) in the Course of Bacterial Meningitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1013"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","1023"],["dc.bibliographiccitation.volume","129"],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","Deeg, S."],["dc.contributor.author","Voigt, A."],["dc.contributor.author","Voßfeldt, H."],["dc.contributor.author","Dohm, C. P."],["dc.contributor.author","Karch, A."],["dc.contributor.author","Weishaupt, Jochen"],["dc.contributor.author","Schulz, J. B."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Kermer, P."],["dc.date.accessioned","2017-09-07T11:46:13Z"],["dc.date.available","2017-09-07T11:46:13Z"],["dc.date.issued","2014"],["dc.description.abstract","Spinocerebellar ataxia type 3 (SCA3) is one of at least nine inherited neurodegenerative diseases caused by an expansion of a polyglutamine tract within corresponding disease-specific proteins. In case of SCA3, mutation of Ataxin-3 results in aggregation of misfolded protein, formation of intranuclear as well as cytosolic inclusion bodies and cell death in distinct neuronal populations. Since cyclin-dependent kinase-5 (CDK5) has been shown to exert beneficial effects on aggregate formation and cell death in various polyglutamine diseases, we tested its therapeutic potential for SCA3. Our data show increased caspase-dependent Ataxin-3 cleavage, aggregation, and neurodegeneration in the absence of sufficient CDK5 activity. This disease-propagating effect could be reversed by mutation of the caspase cleavage site in Ataxin-3. Moreover, reduction of CDK5 expression levels by RNAi in vivo enhances SCA3 toxicity as assayed in a Drosophila model for SCA3. In summary, we present CDK5 as a potent neuroprotectant, regulating cleavage and thereby toxicity of Ataxin-3 and other polyglutamine proteins. We propose that increased caspase-dependent cleavage of mutated Ataxin-3, because of missing CDK5 shielding, leads to aggregation and cell death. Moreover, reduction of CDK5 expression levels by RNAi in vivo enhances SCA3 toxicity as assayed in a Drosophila model for SCA3. We think that CDK5 functions as a shield against cleavage-induced toxification and thereby is an interesting target for therapeutic intervention in polyQ disease in general."],["dc.identifier.doi","10.1111/jnc.12684"],["dc.identifier.gro","3142111"],["dc.identifier.isi","000337760500011"],["dc.identifier.pmid","24548080"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/4666"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1471-4159"],["dc.relation.issn","0022-3042"],["dc.title","CDK5 protects from caspase-induced Ataxin-3 cleavage and neurodegeneration"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","103"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","111"],["dc.bibliographiccitation.volume","255"],["dc.contributor.author","Breit, S."],["dc.contributor.author","Spieker, S."],["dc.contributor.author","Schulz, Joerg B."],["dc.contributor.author","Gasser, Thomas"],["dc.date.accessioned","2018-11-07T11:20:14Z"],["dc.date.available","2018-11-07T11:20:14Z"],["dc.date.issued","2008"],["dc.description.abstract","The differential diagnosis of tremor is mainly based on clinical criteria.Nevertheless, these criteria are in some cases not sufficient to differentiate between different tremor forms. Long-term EMG has proven to be a valid and reliable method for the quantification of pathological tremors. The aim of the study was to develop a long-term EMG-based automated analysis procedure that separates parkinsonian tremor from essential tremor. Using longterm EMG tremor was recorded in 45 consecutive patients, 26 with Parkinson's disease (PD) and 19 with essential tremor (ET). Eight tremor parameters were generated automatically. By stepwise backward regression a subset of these criteria was extracted to achieve an automated classification of the tremor by a mathematical model. The obtained model was then tested on a new group of 13 patients in early stages of the disease. Significant differences between groups were found for tremor occurrence, tremor asymmetry, mean tremor frequency and standard deviation of phase of antagonistic muscles. Due to data overlap a classification of the two tremor forms was not possible based on a single tremor parameter. Using logistic regression, a linear formula based on the three parameters tremor occurrence, mean tremor frequency and standard deviation of phase was established and predicted the correct diagnosis in 93% of patients. The validation of the model on the new group of patients in early stages of the tremor disease yielded a correct diagnosis in 100% of cases. We conclude that long-term EMG recording allows a rater-independent classification of parkinsonian versus essential tremor."],["dc.identifier.doi","10.1007/s00415-008-0712-2"],["dc.identifier.isi","000252674200016"],["dc.identifier.pmid","18204805"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55489"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","0340-5354"],["dc.title","Long-term EMG recordings differentiate between parkinsonian and essential tremor"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.volume","110"],["dc.contributor.author","Butler, Erin K."],["dc.contributor.author","Voigt, Aaron"],["dc.contributor.author","Schulz, Joerg B."],["dc.date.accessioned","2018-11-07T11:25:05Z"],["dc.date.available","2018-11-07T11:25:05Z"],["dc.date.issued","2009"],["dc.format.extent","180"],["dc.identifier.isi","000268550400479"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56553"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell Publishing, Inc"],["dc.publisher.place","Malden"],["dc.relation.conference","22nd Biennial Meeting of the International-Society-of-Neurochemistry/Asian-Pacific-Society-for-Neuroc hemistry"],["dc.relation.eventlocation","Busan, SOUTH KOREA"],["dc.relation.issn","0022-3042"],["dc.title","ALPHA SYNUCLEIN NEUROTOXICITY MODIFIED BY MITOCHONDRIAL CHAPERONE PROTEIN TRAP1"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","225"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neuroscience"],["dc.bibliographiccitation.lastpage","233"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Reich, Arno"],["dc.contributor.author","Spering, Christopher"],["dc.contributor.author","Gertz, Karen"],["dc.contributor.author","Harms, Christoph"],["dc.contributor.author","Gerhardt, Ellen"],["dc.contributor.author","Kronenberg, Golo"],["dc.contributor.author","Nave, Klaus A."],["dc.contributor.author","Schwab, Markus"],["dc.contributor.author","Tauber, Simone C."],["dc.contributor.author","Drinkut, Anja"],["dc.contributor.author","Harms, Kristian"],["dc.contributor.author","Beier, Chrstioph P."],["dc.contributor.author","Voigt, Aaron"],["dc.contributor.author","Goebbels, Sandra"],["dc.contributor.author","Endres, Matthias"],["dc.contributor.author","Schulz, Joerg B."],["dc.date.accessioned","2018-11-07T09:00:08Z"],["dc.date.available","2018-11-07T09:00:08Z"],["dc.date.issued","2011"],["dc.description.abstract","Death receptor (DR) signaling has a major impact on the outcome of numerous neurological diseases, including ischemic stroke. DRs mediate not only cell death signals, but also proinflammatory responses and cell proliferation. Identification of regulatory proteins that control the switch between apoptotic and alternative DR signaling opens new therapeutic opportunities. Fas apoptotic inhibitory molecule 2 (Faim2) is an evolutionary conserved, neuron-specific inhibitor of Fas/CD95-mediated apoptosis. To investigate its role during development and in disease models, we generated Faim2-deficient mice. The ubiquitous null mutation displayed a viable and fertile phenotype without overt deficiencies. However, lack of Faim2 caused an increase in susceptibility to combined oxygen-glucose deprivation in primary neurons in vitro as well as in caspase-associated cell death, stroke volume, and neurological impairment after cerebral ischemia in vivo. These processes were rescued by lentiviral Faim2 gene transfer. In summary, we provide evidence that Faim2 is a novel neuroprotective molecule in the context of cerebral ischemia."],["dc.identifier.doi","10.1523/JNEUROSCI.2188-10.2011"],["dc.identifier.isi","000285915100026"],["dc.identifier.pmid","21209208"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24077"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Soc Neuroscience"],["dc.relation.issn","0270-6474"],["dc.title","Fas/CD95 Regulatory Protein Faim2 Is Neuroprotective after Transient Brain Ischemia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]