Bähr, Mathias

[["dc.bibliographiccitation.firstpage","81"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","93"],["dc.bibliographiccitation.volume","66"],["dc.contributor.author","Gadjanski, Ivana"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Williams, Sarah K."],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Knöferle, Johanna"],["dc.contributor.author","Sättler, Muriel B."],["dc.contributor.author","Fairless, Richard"],["dc.contributor.author","Hochmeister, Sonja"],["dc.contributor.author","Sühs, Kurt-Wolfram"],["dc.contributor.author","Michaelis, Thomas"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Storch, Maria K."],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Diem, Ricarda"],["dc.date.accessioned","2019-07-09T11:52:52Z"],["dc.date.available","2019-07-09T11:52:52Z"],["dc.date.issued","2009"],["dc.description.abstract","Objective: The aim of this study was to investigate the role of voltage-dependent calcium channels (VDCCs) in axon degeneration during autoimmune optic neuritis. Methods: Calcium ion (Ca2 ) influx into the optic nerve (ON) through VDCCs was investigated in a rat model of optic neuritis using manganese-enhanced magnetic resonance imaging and in vivo calcium imaging. After having identified the most relevant channel subtype (N-type VDCCs), we correlated immunohistochemistry of channel expression with ON histopathology. In the confirmatory part of this work, we performed a treatment study using -conotoxin GVIA, an N-type specific blocker. Results: We observed that pathological Ca2 influx into ONs during optic neuritis is mediated via N-type VDCCs. By analyzing the expression of VDCCs in the inflamed ONs, we detected an upregulation of 1B, the pore-forming subunit of N-type VDCCs, in demyelinated axons. However, high expression levels were also found on macrophages/activated microglia, and lower levels were detected on astrocytes. The relevance of N-type VDCCs for inflammation-induced axonal degeneration and the severity of optic neuritis was corroborated by treatment with -conotoxin GVIA. This blocker led to decreased axon and myelin degeneration in the ONs together with a reduced number of macrophages/activated microglia. These protective effects were confirmed by analyzing the spinal cords of the same animals. Interpretation: We conclude that N-type VDCCs play an important role in inflammation-induced axon degeneration via two mechanisms: First, they directly mediate toxic Ca2 influx into the axons; and second, they contribute to macrophage/microglia function, thereby promoting secondary axonal damage."],["dc.identifier.doi","10.1002/ ana.21668"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6088"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60296"],["dc.language.iso","en"],["dc.subject.ddc","610"],["dc.title","Role of N-Type Voltage-Dependent Calcium Channels in Autoimmune Optic Neuritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1232"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Pharmaceuticals"],["dc.bibliographiccitation.lastpage","1240"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","Weishaupt, Jochen H."],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Dietz, Gunnar P. H."],["dc.date.accessioned","2019-07-09T11:53:05Z"],["dc.date.available","2019-07-09T11:53:05Z"],["dc.date.issued","2010"],["dc.description.abstract","Cdk5 is essential for neuronal differentiation processes in the brain. Activation of Cdk5 requires the association with the mostly neuron-specific p35 or p39. Overactivation of CDK5 by cleavage of p35 into p25 is thought to be involved in neurodegenerative processes. Here, we have tested an approach to inhibit pathological Cdk5 activation with a Tat-linked dominant-negative fragment of p25. It reduced cell death induced by staurosporine and showed a tendency to alleviate manganese-induced cell death, while it did not protect against 6-OHDA toxicity. Our results suggest that the Tat technique is a suitable tool to inhibit dysregulated CDK5."],["dc.identifier.doi","10.3390/ph3041232"],["dc.identifier.fs","577416"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6877"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60337"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1424-8247"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Cell-Penetrating Fragments of the Cdk5 Regulatory Subunit Are Protective in Models of Neurodegeneration"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Extracellular Vesicles"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Kuang, Yaoyun"],["dc.contributor.author","Zheng, Xuan"],["dc.contributor.author","Zhang, Lin"],["dc.contributor.author","Ai, Xiaoyu"],["dc.contributor.author","Venkataramani, Vivek"],["dc.contributor.author","Kilic, Ertugrul"],["dc.contributor.author","Hermann, Dirk M."],["dc.contributor.author","Majid, Arshad"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Doeppner, Thorsten R."],["dc.date.accessioned","2021-04-14T08:32:18Z"],["dc.date.available","2021-04-14T08:32:18Z"],["dc.date.issued","2020"],["dc.description.sponsorship","Open-Access-Finanzierung durch die Universitätsmedizin Göttingen 2021"],["dc.identifier.doi","10.1002/jev2.12024"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17797"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83879"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.notes.intern","In goescholar not merged with http://resolver.sub.uni-goettingen.de/purl?gs-1/17840 but duplicate"],["dc.relation.eissn","2001-3078"],["dc.relation.issn","2001-3078"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Adipose‐derived mesenchymal stem cells reduce autophagy in stroke mice by extracellular vesicle transfer of miR‐25"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Clinical and Translational Neuroscience"],["dc.bibliographiccitation.lastpage","5"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Müller, Sebastian J."],["dc.contributor.author","Khadhraoui, Eya"],["dc.contributor.author","Allam, Ibrahim"],["dc.contributor.author","Argyriou, Loukas"],["dc.contributor.author","Hehr, Ute"],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Riedel, Christian H."],["dc.contributor.author","Koch, Jan C."],["dc.date.accessioned","2020-05-28T12:53:29Z"],["dc.date.accessioned","2021-10-27T13:22:13Z"],["dc.date.available","2020-05-28T12:53:29Z"],["dc.date.available","2021-10-27T13:22:13Z"],["dc.date.issued","2020"],["dc.description.abstract","Cerebral Autosomal Recessive Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CARASIL, Maedasyndrome) is an extremely rare autosomal-recessive genetic disorder with a serious arteriopathy causing subcorticalinfarcts and leukoencephalopathy. In less than 20 cases, a genetic mutation was proven. Patients suffer from alopecia, discherniations, and spondylosis. Between the age of 30 and 40, the patients typically develop severe cerebral infarcts. Clinicalsymptoms, genetic study, magnetic resonance imaging (MRI), and coronary angiography of a patient with proven CARASILare presented. The patient showed the typical phenotype with cerebral small-vessel disease, cerebral infarcts, spondylosis,and abnormal hair loss. Additionally, distinct cerebral microhemorrhage and a severe coronary artery disease (CAD)were found, which have not been reported before for CARASIL. Mutation screening revealed the presence of ahomozygous c.1022G > T substitution in the HTRA1 gene. Evidence from other publications supports a pathogenetic linkbetween the HTRA1 mutation and CAD as a new feature of CARASIL. This is the first report about CARASIL with aconcomitant severe CAD. Thus, in patients with CARASIL, other vessel diseases should also be considered."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2020"],["dc.identifier.doi","10.1177/2514183X20914182"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17348"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92075"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","2514-183X"],["dc.relation.issn","2514-183X"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","CARASIL with coronary artery disease and distinct cerebral microhemorrhage: A case report and literature review"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","49"],["dc.bibliographiccitation.journal","Frontiers in Molecular Neuroscience"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Tolö, Johan"],["dc.contributor.author","Taschenberger, Grit"],["dc.contributor.author","Leite, Kristian"],["dc.contributor.author","Stahlberg, Markus A."],["dc.contributor.author","Spehlbrink, Gesche"],["dc.contributor.author","Kues, Janina"],["dc.contributor.author","Munari, Francesca"],["dc.contributor.author","Capaldi, Stefano"],["dc.contributor.author","Becker, Stefan"],["dc.contributor.author","Zweckstetter, Markus"],["dc.contributor.author","Dean, Camin"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Kügler, Sebastian"],["dc.date.accessioned","2019-07-09T11:45:10Z"],["dc.date.available","2019-07-09T11:45:10Z"],["dc.date.issued","2018"],["dc.description.abstract","α-Synuclein (α-Syn) is intimately linked to the etiology of Parkinson's Disease, as mutations and even subtle increases in gene dosage result in early onset of the disease. However, how this protein causes neuronal dysfunction and neurodegeneration is incompletely understood. We thus examined a comprehensive range of physiological parameters in cultured rat primary neurons overexpressing α-Syn at levels causing a slowly progressive neurodegeneration. In contradiction to earlier reports from non-neuronal assay systems we demonstrate that α-Syn does not interfere with essential ion handling capacities, mitochondrial capability of ATP production or basic electro-physiological properties like resting membrane potential or the general ability to generate action potentials. α-Syn also does not activate canonical stress kinase Signaling converging on SAPK/Jun, p38 MAPK or Erk kinases. Causative for α-Syn-induced neurodegeneration are mitochondrial thiol oxidation and activation of caspases downstream of mitochondrial outer membrane permeabilization, leading to apoptosis-like cell death execution with some unusual aspects. We also aimed to elucidate neuroprotective strategies counteracting the pathophysiological processes caused by α-Syn. Neurotrophic factors, calpain inhibition and increased lysosomal protease capacity showed no protective effects against α-Syn overexpression. In contrast, the major watchdog of outer mitochondrial membrane integrity, Bcl-Xl, was capable of almost completely preventing neuron death, but did not prevent mitochondrial thiol oxidation. Importantly, independent from the quite mono-causal induction of neurotoxicity, α-Syn causes diminished excitability of neurons by external stimuli and robust impairments in endogenous neuronal network activity by decreasing the frequency of action potentials generated without external stimulation. This latter finding suggests that α-Syn can induce neuronal dysfunction independent from its induction of neurotoxicity and might serve as an explanation for functional deficits that precede neuronal cell loss in synucleopathies like Parkinson's disease or dementia with Lewy bodies."],["dc.identifier.doi","10.3389/fnmol.2018.00049"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15047"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59171"],["dc.language.iso","en"],["dc.notes.intern","DeepGreen Import"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","1662-5099"],["dc.relation.issn","1662-5099"],["dc.rights","http://creativecommons.org/licenses/by/4.0/"],["dc.subject.ddc","610"],["dc.title","Pathophysiological Consequences of Neuronal α-Synuclein Overexpression: Impacts on Ion Homeostasis, Stress Signaling, Mitochondrial Integrity, and Electrical Activity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","101639"],["dc.bibliographiccitation.journal","NeuroImage Clinical"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Maier, Ilko L."],["dc.contributor.author","Hofer, Sabine"],["dc.contributor.author","Joseph, Arun A."],["dc.contributor.author","Merboldt, K.-Dietmar"],["dc.contributor.author","Eggert, Eva"],["dc.contributor.author","Behme, Daniel"],["dc.contributor.author","Schregel, Katharina"],["dc.contributor.author","Brelie, Christian von der"],["dc.contributor.author","Rohde, Veit"],["dc.contributor.author","Koch, Jan-Christoph"],["dc.contributor.author","Psychogios, Marios-Nikos"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","Bähr, Mathias"],["dc.date.accessioned","2019-07-09T11:50:09Z"],["dc.date.available","2019-07-09T11:50:09Z"],["dc.date.issued","2019"],["dc.description.abstract","BACKGROUND: Degenerative changes of the cervical spinal column are the most common cause of spinal cord lesions in the elderly. Conventional clinical, electrophysiological and radiological diagnostics of spinal cord compression are often inconsistent. MATERIALS AND METHODS: The feasibility and diagnostic potential of a novel T1 mapping method at 0.5 mm resolution and 4 s acquisition time was evaluated in 14 patients with degenerative cervical spinal canal stenosis (SCS) and 6 healthy controls. T1 mapping was performed in axial sections of the stenosis as well as above and below. All subjects received standard T2-weighted MRI of the cervical spine (including SCS-grading 0-III), electrophysiological and clinical examinations. RESULTS: Patients revealed significantly decreased T1 relaxation times of the compressed spinal cord within the SCS (912 ± 53 ms, mean ± standard deviation) in comparison to unaffected segments above (1027 ± 39 ms, p < .001) and below (1056 ± 93 ms, p < .001). There was no difference in mean T1 in unaffected segments in patients (p = .712) or between segments in controls (p = .443). Moreover, T1 values were significantly lower in grade II (881 ± 46 ms, p = .005) than in grade I SCS (954 ± 29 ms). Patients with central conduction deficit tended to have lower T1 values within the SCS than patients without (909 ± 50 ms vs 968 ± 7 ms, p = .069). CONCLUSION: Rapid high-resolution T1 mapping is a robust MRI method for quantifying spinal cord compression in patients with cervical SCS. It promises additional diagnostic insights and warrants more extended patient studies."],["dc.identifier.doi","10.1016/j.nicl.2018.101639"],["dc.identifier.pmid","30553763"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15872"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59713"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2213-1582"],["dc.rights","CC BY-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nd/4.0"],["dc.subject.ddc","610"],["dc.title","Quantification of spinal cord compression using T1 mapping in patients with cervical spinal canal stenosis - Preliminary experience"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","BMC Neuroscience"],["dc.contributor.author","Weishaupt, Jochen Hans"],["dc.contributor.author","Dietz, Gunnar"],["dc.contributor.author","Göricke, Bettina"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Frank, Tobias"],["dc.contributor.author","Schlachetzki, Johannes C. M."],["dc.contributor.author","Meuer, Katrin"],["dc.contributor.author","Rohde, Gundula"],["dc.contributor.author","Schneider, Armin"],["dc.date.accessioned","2019-07-10T08:13:27Z"],["dc.date.available","2019-07-10T08:13:27Z"],["dc.date.issued","2009"],["dc.description.abstract","Background: The hematopoietic Granulocyte-Colony Stimulating Factor (G-CSF) plays a crucial role in controlling the number of neutrophil progenitor cells. Its function is mediated via the G-CSF receptor, which was recently found to be expressed also in the central nervous system. In addition, G-CSF provided neuroprotection in models of neuronal cell death. Here we used the retinal ganglion cell (RGC) axotomy model to compare effects of local and systemic application of neuroprotective molecules. Results: We found that the G-CSF receptor is robustly expressed by RGCs in vivo and in vitro. We thus evaluated G-CSF as a neuroprotectant for RGCs and found a dose-dependent neuroprotective effect of G-CSF on axotomized RGCs when given subcutaneously. As stem stell mobilization had previously been discussed as a possible contributor to the neuroprotective effects of G-CSF, we compared the local treatment of RGCs by injection of G-CSF into the vitreous body with systemic delivery by subcutaneous application. Both routes of application reduced retinal ganglion cell death to a comparable extent. Moreover, G-CSF enhanced the survival of immunopurified RGCs in vitro. Conclusion: We thus show that G-CSF neuroprotection is at least partially independent of potential systemic effects and provide further evidence that the clinically applicable G-CSF could become a treatment option for both neurodegenerative diseases and glaucoma"],["dc.identifier.fs","568091"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5954"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/61250"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1471-2202"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Both systemic and local application of granulocyte-colony stimulating factor (G-CSF) is neuroprotective after retinal ganglion cell axotomy."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]