Koch, Jan-Christoph

[["dc.bibliographiccitation.firstpage","289"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Cell and Tissue Research"],["dc.bibliographiccitation.lastpage","311"],["dc.bibliographiccitation.volume","349"],["dc.contributor.author","Lingor, P."],["dc.contributor.author","Koch, J. C."],["dc.contributor.author","Tönges, L."],["dc.contributor.author","Bähr, M."],["dc.date.accessioned","2017-09-07T11:48:50Z"],["dc.date.available","2017-09-07T11:48:50Z"],["dc.date.issued","2012"],["dc.description.abstract","Degeneration of the axon is an important step in the pathomechanism of traumatic, inflammatory and degenerative neurological diseases. Increasing evidence suggests that axonal degeneration occurs early in the course of these diseases and therefore represents a promising target for future therapeutic strategies. We review the evidence for axonal destruction from pathological findings and animal models with particular emphasis on neurodegenerative and neurotraumatic disorders. We discuss the basic morphological and temporal modalities of axonal degeneration (acute, chronic and focal axonal degeneration and Wallerian degeneration). Based on the mechanistic concepts, we then delineate in detail the major molecular mechanisms that underlie the degenerative cascade, such as calcium influx, axonal transport, protein aggregation and autophagy. We finally concentrate on putative therapeutic targets based on the mechanistic prerequisites."],["dc.identifier.doi","10.1007/s00441-012-1362-3"],["dc.identifier.gro","3142506"],["dc.identifier.isi","000305405800023"],["dc.identifier.pmid","22392734"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8101"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8865"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0302-766X"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject","Neurodegeneration; Neurotrauma; Wallerian degeneration; Calcium Autophagy"],["dc.title","Axonal degeneration as a therapeutic target in the CNS"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e1811"],["dc.bibliographiccitation.journal","Cell Death and Disease"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Koch, J. C."],["dc.contributor.author","Bitow, F."],["dc.contributor.author","Haack, J."],["dc.contributor.author","D'Hedouville, Z."],["dc.contributor.author","Zhang, J-N"],["dc.contributor.author","Tönges, L."],["dc.contributor.author","Michel, U."],["dc.contributor.author","Oliveira, L. M. A."],["dc.contributor.author","Jovin, T. M."],["dc.contributor.author","Liman, Jan"],["dc.contributor.author","Tatenhorst, L."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Lingor, P."],["dc.date.accessioned","2017-09-07T11:43:42Z"],["dc.date.available","2017-09-07T11:43:42Z"],["dc.date.issued","2015"],["dc.description.abstract","Many neuropathological and experimental studies suggest that the degeneration of dopaminergic terminals and axons precedes the demise of dopaminergic neurons in the substantia nigra, which finally results in the clinical symptoms of Parkinson disease (PD). The mechanisms underlying this early axonal degeneration are, however, still poorly understood. Here, we examined the effects of overexpression of human wildtype alpha-synuclein (alpha Syn-WT), a protein associated with PD, and its mutant variants alpha Syn-A30P and -A53T on neurite morphology and functional parameters in rat primary midbrain neurons (PMN). Moreover, axonal degeneration after overexpression of alpha Syn-WT and -A30P was analyzed by live imaging in the rat optic nerve in vivo. We found that overexpression of alpha Syn-WT and of its mutants A30P and A53T impaired neurite outgrowth of PMN and affected neurite branching assessed by Sholl analysis in a variant-dependent manner. Surprisingly, the number of primary neurites per neuron was increased in neurons transfected with alpha Syn. Axonal vesicle transport was examined by live imaging of PMN co-transfected with EGFP-labeled synaptophysin. Overexpression of all alpha Syn variants significantly decreased the number of motile vesicles and decelerated vesicle transport compared with control. Macroautophagic flux in PMN was enhanced by alpha Syn-WT and -A53T but not by alpha Syn-A30P. Correspondingly, colocalization of alpha Syn and the autophagy marker LC3 was reduced for alpha Syn-A30P compared with the other alpha Syn variants. The number of mitochondria colocalizing with LC3 as a marker for mitophagy did not differ among the groups. In the rat optic nerve, both alpha Syn-WT and -A30P accelerated kinetics of acute axonal degeneration following crush lesion as analyzed by in vivo live imaging. We conclude that alpha Syn overexpression impairs neurite outgrowth and augments axonal degeneration, whereas axonal vesicle transport and autophagy are severely altered."],["dc.description.sponsorship","Open-Access Publikationsfonds 2015"],["dc.identifier.doi","10.1038/cddis.2015.169"],["dc.identifier.gro","3141868"],["dc.identifier.isi","000358788800011"],["dc.identifier.pmid","26158517"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12015"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1967"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","2041-4889"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject","Central nervous system; Molecular neuroscience; Parkinson's disease"],["dc.title","Alpha-Synuclein affects neurite morphology, autophagy, vesicle transport and axonal degeneration in CNS neurons"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","39"],["dc.bibliographiccitation.journal","Frontiers in Molecular Neuroscience"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Tönges, L."],["dc.contributor.author","Koch, J.-C."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Lingor, P."],["dc.date.accessioned","2017-09-07T11:45:03Z"],["dc.date.available","2017-09-07T11:45:03Z"],["dc.date.issued","2011"],["dc.description.abstract","Regenerative failure in the CNS largely depends on pronounced growth inhibitory signaling and reduced cellular survival after a lesion stimulus. One key mediator of growth inhibitory signaling is Rho-associated kinase (ROCK), which has been shown to modulate growth cone stability by regulation of actin dynamics. Recently, there is accumulating evidence the ROCK also plays a deleterious role for cellular survival. In this manuscript we illustrate that ROCK is involved in a variety of intracellular signaling pathways that comprise far more than those involved in neurite growth inhibition alone. Although ROCK function is currently studied in many different disease contexts, our review focuses on neurorestorative approaches in the CNS, especially in models of neurotrauma. Promising strategies to target ROCK by pharmacological small molecule inhibitors and RNAi approaches are evaluated for their outcome on regenerative growth and cellular protection both in preclinical and in clinical studies."],["dc.identifier.doi","10.3389/fnmol.2011.00039"],["dc.identifier.gro","3142797"],["dc.identifier.isi","000209370100036"],["dc.identifier.pmid","22065949"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8272"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/241"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1662-5099"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","ROCKing regeneration: Rho kinase inhibition as molecular target for neurorestoration"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3355"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","3370"],["dc.bibliographiccitation.volume","135"],["dc.contributor.author","Tönges, L."],["dc.contributor.author","Frank, T."],["dc.contributor.author","Tatenhorst, L."],["dc.contributor.author","Saal, K. A."],["dc.contributor.author","Koch, J. C."],["dc.contributor.author","Szego, E. M."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Weishaupt, J. H."],["dc.contributor.author","Lingor, P."],["dc.date.accessioned","2017-09-07T11:48:22Z"],["dc.date.available","2017-09-07T11:48:22Z"],["dc.date.issued","2012"],["dc.description.abstract","Axonal degeneration is one of the earliest features of Parkinson's disease pathology, which is followed by neuronal death in the substantia nigra and other parts of the brain. Inhibition of axonal degeneration combined with cellular neuroprotection therefore seem key to targeting an early stage in Parkinson's disease progression. Based on our previous studies in traumatic and neurodegenerative disease models, we have identified rho kinase as a molecular target that can be manipulated to disinhibit axonal regeneration and improve survival of lesioned central nervous system neurons. In this study, we examined the neuroprotective potential of pharmacological rho kinase inhibition mediated by fasudil in the in vitro 1-methyl-4-phenylpyridinium cell culture model and in the subchronic in vivo 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson's disease. Application of fasudil resulted in a significant attenuation of dopaminergic cell loss in both paradigms. Furthermore, dopaminergic terminals were preserved as demonstrated by analysis of neurite network in vitro, striatal fibre density and by neurochemical analysis of the levels of dopamine and its metabolites in the striatum. Behavioural tests demonstrated a clear improvement in motor performance after fasudil treatment. The Akt survival pathway was identified as an important molecular mediator for neuroprotective effects of rho kinase inhibition in our paradigm. We conclude that inhibition of rho kinase using the clinically approved small molecule inhibitor fasudil may be a promising new therapeutic strategy for Parkinson's disease."],["dc.identifier.doi","10.1093/brain/aws254"],["dc.identifier.gro","3142444"],["dc.identifier.isi","000311644800021"],["dc.identifier.pmid","23087045"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9499"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8352"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0006-8950"],["dc.rights","CC BY-NC 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/3.0"],["dc.title","Inhibition of rho kinase enhances survival of dopaminergic neurons and attenuates axonal loss in a mouse model of Parkinson's disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","304"],["dc.bibliographiccitation.journal","Frontiers in Neuroscience"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Günther, R."],["dc.contributor.author","Saal, K.-A."],["dc.contributor.author","Suhr, M."],["dc.contributor.author","Scheer, D."],["dc.contributor.author","Koch, J. C."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Lingor, P."],["dc.contributor.author","Tönges, L."],["dc.date.accessioned","2017-09-07T11:45:27Z"],["dc.date.available","2017-09-07T11:45:27Z"],["dc.date.issued","2014"],["dc.description.abstract","Disease progression in amyotrophic lateral sclerosis (ALS) is characterized by degeneration of motoneurons and their axons which results in a progressive muscle weakness and ultimately death from respiratory failure. The only approved drug, riluzole, lacks clinical efficacy so that more potent treatment options are needed. We have identified rho kinase (ROCK) as a target, which can be manipulated to beneficially influence disease progression in models of ALS. Here, we examined the therapeutic potential of the ROCK inhibitor Y-27632 in both an in vitro and in an in vivo paradigm of motoneuron disease. Application of Y-27632 to primary motoneurons in vitro increased survival and promoted neunte outgrowth. In vivo, SOD1G93A mice were orally treated with 2 or 30 mg/kg body weight of Y-27632. The 2 mg/kg group did not benefit from Y-27632 treatment, whereas treatment with 30 mg/kg resulted in improved motor function in male mice. Female mice showed only limited improvement and overall survival was not modified in both 2 and 30 mg/kg Y-27632 groups. In conclusion, we provide evidence that inhibition of ROCK by Y-27632 is neuroprotective in vitro but has limited beneficial effects in vivo being restricted to male mice. Therefore, the evaluation of ROCK inhibitors in preclinical models of ALS should always take gender differences into account."],["dc.format.extent","9"],["dc.identifier.doi","10.3389/fnins.2014.00304"],["dc.identifier.gro","3142033"],["dc.identifier.isi","000346516800001"],["dc.identifier.pmid","25339858"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11029"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/3801"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1662-453X"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","The rho kinase inhibitor Y-27632 improves motor performance in male SOD1(G93A) mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e1994"],["dc.bibliographiccitation.journal","Cell Death and Disease"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Oliveira, Luis M. A."],["dc.contributor.author","Falomir-Lockhart, Lisandro J."],["dc.contributor.author","Botelho, Michelle Gralle"],["dc.contributor.author","Lin, K-H"],["dc.contributor.author","Wales, Pauline"],["dc.contributor.author","Koch, Jan Christoph"],["dc.contributor.author","Gerhardt, Ellen"],["dc.contributor.author","Taschenberger, Holger"],["dc.contributor.author","Outeiro, Tiago Fleming"],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Schuele, B."],["dc.contributor.author","Arndt-Jovin, Donna J."],["dc.contributor.author","Jovin, Thomas M."],["dc.date.accessioned","2018-11-07T09:49:15Z"],["dc.date.available","2018-11-07T09:49:15Z"],["dc.date.issued","2015"],["dc.description.abstract","We have assessed the impact of alpha-synuclein overexpression on the differentiation potential and phenotypic signatures of two neural-committed induced pluripotent stem cell lines derived from a Parkinson's disease patient with a triplication of the human SNCA genomic locus. In parallel, comparative studies were performed on two control lines derived from healthy individuals and lines generated from the patient iPS-derived neuroprogenitor lines infected with a lentivirus incorporating a small hairpin RNA to knock down the SNCA mRNA. The SNCA triplication lines exhibited a reduced capacity to differentiate into dopaminergic or GABAergic neurons and decreased neurite outgrowth and lower neuronal activity compared with control cultures. This delayed maturation phenotype was confirmed by gene expression profiling, which revealed a significant reduction in mRNA for genes implicated in neuronal differentiation such as delta-like homolog 1 (DLK1), gamma-aminobutyric acid type B receptor subunit 2 (GABABR2), nuclear receptor related 1 protein (NURR1), G-protein-regulated inward-rectifier potassium channel 2 (GIRK-2) and tyrosine hydroxylase (TH). The differentiated patient cells also demonstrated increased autophagic flux when stressed with chloroquine. We conclude that a two-fold overexpression of alpha-synuclein caused by a triplication of the SNCA gene is sufficient to impair the differentiation of neuronal progenitor cells, a finding with implications for adult neurogenesis and Parkinson's disease progression, particularly in the context of bioenergetic dysfunction."],["dc.identifier.doi","10.1038/cddis.2015.318"],["dc.identifier.isi","000367155300027"],["dc.identifier.pmid","26610207"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12755"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35470"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","2041-4889"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Elevated alpha-synuclein caused by SNCA gene triplication impairs neuronal differentiation and maturation in Parkinson's patient-derived induced pluripotent stem cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","175628641984605"],["dc.bibliographiccitation.journal","Therapeutic Advances in Neurological Disorders"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Wurster, Claudia D."],["dc.contributor.author","Günther, René"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Dreyhaupt, Jens"],["dc.contributor.author","Wollinsky, Kurt"],["dc.contributor.author","Uzelac, Zeljko"],["dc.contributor.author","Witzel, Simon"],["dc.contributor.author","Kocak, Tugrul"],["dc.contributor.author","Winter, Benedikt"],["dc.contributor.author","Koch, Jan C."],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Petri, Susanne"],["dc.contributor.author","Ludolph, Albert C."],["dc.contributor.author","Hermann, Andreas"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2020-12-10T18:38:37Z"],["dc.date.available","2020-12-10T18:38:37Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1177/1756286419846058"],["dc.identifier.eissn","1756-2864"],["dc.identifier.issn","1756-2864"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16746"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77390"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","Neurochemical markers in CSF of adolescent and adult SMA patients undergoing nusinersen treatment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","692"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Neural Regeneration Research"],["dc.bibliographiccitation.lastpage","+"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Zhang, J."],["dc.contributor.author","Koch, Jan Christoph"],["dc.date.accessioned","2018-11-07T10:24:02Z"],["dc.date.available","2018-11-07T10:24:02Z"],["dc.date.issued","2017"],["dc.description.abstract","Axonal degeneration is a key pathological feature in many neurological diseases. It often leads to persistent deficits due to the inability of axons to regenerate in the central nervous system. Therefore therapeutic approaches should optimally both attenuate axonal degeneration and foster axonal regeneration. Compelling evidence suggests that collapsin response mediator protein-2 (CRMP2) might be a molecular target fulfilling these requirements. In this mini-review, we give a compact overview of the known functions of CRMP2 and its molecular interactors in neurite outgrowth and in neurodegenerative conditions. Moreover, we discuss in detail our recent findings on the role of CRMP2 in acute axonal degeneration in the optic nerve. We found that the calcium influx induced by the lesion activates the protease calpain which cleaves CRMP2, leading to impairment of axonal transport. Both calpain inhibition and CRMP2 overexpression effectively protected the proximal axons against acute axonal degeneration. Taken together, CRMP2 is further characterized as a central molecular player in acute axonal degeneration and thus evolves as a promising therapeutic target to both counteract axonal degeneration and foster axonal regeneration in neurodegenerative and neurotraumatic diseases."],["dc.identifier.doi","10.4103/1673-5374.206631"],["dc.identifier.isi","000403378800004"],["dc.identifier.pmid","28616018"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14962"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42581"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Medknow Publications & Media Pvt Ltd"],["dc.relation.issn","1876-7958"],["dc.relation.issn","1673-5374"],["dc.rights","CC BY-NC-SA 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-sa/3.0"],["dc.title","Collapsin response mediator protein-2 plays a major protective role in acute axonal degeneration"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3935"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.volume","23"],["dc.contributor.affiliation","Dias, Mariana Santana; 1Intermediate Laboratory of Gene Therapy and Viral Vectors, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Rio de Janeiro 21941-902, Brazil; mdias@biof.ufrj.br (M.S.D.); hilda@biof.ufrj.br (H.P.-S.)"],["dc.contributor.affiliation","Luo, Xiaoyue; 2Department of Neurology, University Medical Center Göttingen, 37077 Göttingen, Germany; xiaoyue.luo@med.uni-goettingen.de"],["dc.contributor.affiliation","Ribas, Vinicius Toledo; 3Laboratory of Neurobiology, Department of Morphology, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte 31270-901, Brazil; ribasvt@ufmg.br"],["dc.contributor.affiliation","Petrs-Silva, Hilda; 1Intermediate Laboratory of Gene Therapy and Viral Vectors, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Rio de Janeiro 21941-902, Brazil; mdias@biof.ufrj.br (M.S.D.); hilda@biof.ufrj.br (H.P.-S.)"],["dc.contributor.affiliation","Koch, Jan Christoph; 2Department of Neurology, University Medical Center Göttingen, 37077 Göttingen, Germany; xiaoyue.luo@med.uni-goettingen.de"],["dc.contributor.author","Dias, Mariana Santana"],["dc.contributor.author","Luo, Xiaoyue"],["dc.contributor.author","Ribas, Vinicius Toledo"],["dc.contributor.author","Petrs-Silva, Hilda"],["dc.contributor.author","Koch, Jan Christoph"],["dc.date.accessioned","2022-05-02T08:09:37Z"],["dc.date.available","2022-05-02T08:09:37Z"],["dc.date.issued","2022"],["dc.date.updated","2022-09-03T21:04:55Z"],["dc.description.abstract","Glaucoma is a neurodegenerative disease that affects the retinal ganglion cells (RGCs) and leads to progressive vision loss. The first pathological signs can be seen at the optic nerve head (ONH), the structure where RGC axons leave the retina to compose the optic nerve. Besides damage of the axonal cytoskeleton, axonal transport deficits at the ONH have been described as an important feature of glaucoma. Axonal transport is essential for proper neuronal function, including transport of organelles, synaptic components, vesicles, and neurotrophic factors. Impairment of axonal transport has been related to several neurodegenerative conditions. Studies on axonal transport in glaucoma include analysis in different animal models and in humans, and indicate that its failure happens mainly in the ONH and early in disease progression, preceding axonal and somal degeneration. Thus, a better understanding of the role of axonal transport in glaucoma is not only pivotal to decipher disease mechanisms but could also enable early therapies that might prevent irreversible neuronal damage at an early time point. In this review we present the current evidence of axonal transport impairment in glaucomatous neurodegeneration and summarize the methods employed to evaluate transport in this disease."],["dc.description.abstract","Glaucoma is a neurodegenerative disease that affects the retinal ganglion cells (RGCs) and leads to progressive vision loss. The first pathological signs can be seen at the optic nerve head (ONH), the structure where RGC axons leave the retina to compose the optic nerve. Besides damage of the axonal cytoskeleton, axonal transport deficits at the ONH have been described as an important feature of glaucoma. Axonal transport is essential for proper neuronal function, including transport of organelles, synaptic components, vesicles, and neurotrophic factors. Impairment of axonal transport has been related to several neurodegenerative conditions. Studies on axonal transport in glaucoma include analysis in different animal models and in humans, and indicate that its failure happens mainly in the ONH and early in disease progression, preceding axonal and somal degeneration. Thus, a better understanding of the role of axonal transport in glaucoma is not only pivotal to decipher disease mechanisms but could also enable early therapies that might prevent irreversible neuronal damage at an early time point. In this review we present the current evidence of axonal transport impairment in glaucomatous neurodegeneration and summarize the methods employed to evaluate transport in this disease."],["dc.identifier.doi","10.3390/ijms23073935"],["dc.identifier.pii","ijms23073935"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107420"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-561"],["dc.relation.eissn","1422-0067"],["dc.rights","CC BY 4.0"],["dc.title","The Role of Axonal Transport in Glaucoma"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","372"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Brain Sciences"],["dc.bibliographiccitation.volume","11"],["dc.contributor.affiliation","Peseschkian, Tara; \t\t \r\n\t\t Department of Neurology, Hannover Medical School, 30625 Hannover, Germany, Peseschkian.Tara@mh-hannover.de"],["dc.contributor.affiliation","Cordts, Isabell; \t\t \r\n\t\t Department of Neurology, Klinikum Rechts der Isar, Technical University of Munich, 81675 Munich, Germany, isabell.cordts@tum.de"],["dc.contributor.affiliation","Günther, René; \t\t \r\n\t\t Department of Neurology, University Hospital Carl Gustav Carus, 01307 Dresden, Germany, Rene.Guenther@uniklinikum-dresden.de\t\t \r\n\t\t German Center for Neurodegenerative Diseases (DZNE), 01307 Dresden, Germany, Rene.Guenther@uniklinikum-dresden.de"],["dc.contributor.affiliation","Stolte, Benjamin; \t\t \r\n\t\t Department of Neurology, University Medicine Essen, 45147 Essen, Germany, benjamin.stolte@uk-essen.de"],["dc.contributor.affiliation","Zeller, Daniel; \t\t \r\n\t\t Department of Neurology, University of Würzburg, 97080 Würzburg, Germany, Zeller_D@ukw.de"],["dc.contributor.affiliation","Schröter, Carsten; \t\t \r\n\t\t Hoher Meißner Clinic, Neurology, 37242 Bad Sooden-Allendorf, Germany, Schroeter@reha-klinik.de"],["dc.contributor.affiliation","Weyen, Ute; \t\t \r\n\t\t Department of Neurology, Ruhr-University Bochum, BG-Kliniken Bergmannsheil, 44789 Bochum, Germany, ute.weyen@bergmannsheil.de"],["dc.contributor.affiliation","Regensburger, Martin; \t\t \r\n\t\t Department of Molecular Neurology, Friedrich-Alexander-University Erlangen-Nürnberg, 91054 Erlangen, Germany, Martin.Regensburger@uk-erlangen.de"],["dc.contributor.affiliation","Wolf, Joachim; \t\t \r\n\t\t Department of Neurology, Diakonissen Hospital Mannheim, 68163 Mannheim, Germany, j.wolf@diako-mannheim.de"],["dc.contributor.affiliation","Schneider, Ilka; \t\t \r\n\t\t Department of Neurology, Martin-Luther University Halle/Saale, 06120 Halle, Germany, Ilka.Schneider@sanktgeorg.de\t\t \r\n\t\t Department of Neurology, Klinikum Sankt Georg, 04129 Leipzig, Germany, Ilka.Schneider@sanktgeorg.de"],["dc.contributor.affiliation","Hermann, Andreas; \t\t \r\n\t\t Translational Neurodegeneration Section “Albrecht-Kossel”, Department of Neurology, University Medical Center Rostock, University of Rostock, 18147 Rostock, Germany, Andreas.Hermann@med.uni-rostock.de\t\t \r\n\t\t German Center for Neurodegenerative Diseases Rostock/Greifswald, 18147 Rostock, Germany, Andreas.Hermann@med.uni-rostock.de"],["dc.contributor.affiliation","Metelmann, Moritz; \t\t \r\n\t\t Department of Neurology, University Hospital Leipzig, 04103 Leipzig, Germany, Moritz.Metelmann@medizin.uni-leipzig.de"],["dc.contributor.affiliation","Kohl, Zacharias; \t\t \r\n\t\t Department of Neurology, University of Regensburg, 93053 Regensburg, Germany, zacharias.kohl@klinik.uni-regensburg.de"],["dc.contributor.affiliation","Linker, Ralf A.; \t\t \r\n\t\t Department of Neurology, University of Regensburg, 93053 Regensburg, Germany, Ralf.Linker@klinik.uni-regensburg.de"],["dc.contributor.affiliation","Koch, Jan Christoph; \t\t \r\n\t\t Department of Neurology, University Medicine Göttingen, 37075 Göttingen, Germany, jkoch@med.uni-goettingen.de"],["dc.contributor.affiliation","Büchner, Boriana; \t\t \r\n\t\t Friedrich-Baur Institute, Department of Neurology, University Hospital, Ludwig Maximilian University of Munich, 80336 Munich, Germany, Boriana.Buechner@med.uni-muenchen.de"],["dc.contributor.affiliation","Weiland, Ulrike; \t\t \r\n\t\t Department of Neurology, University of Ulm, 89081 Ulm, Germany, Ulrike.Weiland@uniklinik-ulm.de"],["dc.contributor.affiliation","Schönfelder, Erik; \t\t \r\n\t\t Department of Neurology, Hannover Medical School, 30625 Hannover, Germany, Erik.Schoenfelder@stud.mh-hannover.de"],["dc.contributor.affiliation","Heinrich, Felix; \t\t \r\n\t\t Department of Neurology, Hannover Medical School, 30625 Hannover, Germany, Felix.Heinrich@stud.mh-hannover.de"],["dc.contributor.affiliation","Osmanovic, Alma; \t\t \r\n\t\t Department of Neurology, Hannover Medical School, 30625 Hannover, Germany, dr.almaosmanovic@gmail.com"],["dc.contributor.affiliation","Klopstock, Thomas; \t\t \r\n\t\t Friedrich-Baur Institute, Department of Neurology, University Hospital, Ludwig Maximilian University of Munich, 80336 Munich, Germany, Thomas.Klopstock@med.uni-muenchen.de\t\t \r\n\t\t Munich Cluster for Systems Neurology (SyNergy), 80336 Munich, Germany, Thomas.Klopstock@med.uni-muenchen.de\t\t \r\n\t\t German Center for Neurodegenerative Diseases (DZNE), 80336 Munich, Germany, Thomas.Klopstock@med.uni-muenchen.de"],["dc.contributor.affiliation","Dorst, Johannes; \t\t \r\n\t\t Department of Neurology, University of Ulm, 89081 Ulm, Germany, johannes.dorst@rku.de"],["dc.contributor.affiliation","Ludolph, Albert C.; \t\t \r\n\t\t Department of Neurology, University of Ulm, 89081 Ulm, Germany, albert.ludolph@rku.de\t\t \r\n\t\t German Center for Neurodegenerative Diseases (DZNE), 89081 Ulm, Germany, albert.ludolph@rku.de"],["dc.contributor.affiliation","Boentert, Matthias; \t\t \r\n\t\t Department of Neurology with the Institute of Translational Neurology, University Hospital Münster, 48149 Münster, Germany, Matthias.Boentert@ukmuenster.de\t\t \r\n\t\t Department of Medicine, UKM Marienhospital, 48565 Steinfurt, Germany, Matthias.Boentert@ukmuenster.de"],["dc.contributor.affiliation","Hagenacker, Tim; \t\t \r\n\t\t Department of Neurology, University Medicine Essen, 45147 Essen, Germany, tim.hagenacker@uk-essen.de"],["dc.contributor.affiliation","Deschauer, Marcus; \t\t \r\n\t\t Department of Neurology, Klinikum Rechts der Isar, Technical University of Munich, 81675 Munich, Germany, marcus.deschauer@mri.tum.de"],["dc.contributor.affiliation","Lingor, Paul; \t\t \r\n\t\t Department of Neurology, Klinikum Rechts der Isar, Technical University of Munich, 81675 Munich, Germany, paul.lingor@tum.de"],["dc.contributor.affiliation","Petri, Susanne; \t\t \r\n\t\t Department of Neurology, Hannover Medical School, 30625 Hannover, Germany, Petri.Susanne@mh-hannover.de"],["dc.contributor.affiliation","Schreiber-Katz, Olivia; \t\t \r\n\t\t Department of Neurology, Hannover Medical School, 30625 Hannover, Germany, Schreiber-Katz.Olivia@mh-hannover.de"],["dc.contributor.author","Peseschkian, Tara"],["dc.contributor.author","Cordts, Isabell"],["dc.contributor.author","Günther, René"],["dc.contributor.author","Stolte, Benjamin"],["dc.contributor.author","Zeller, Daniel"],["dc.contributor.author","Schröter, Carsten"],["dc.contributor.author","Weyen, Ute"],["dc.contributor.author","Regensburger, Martin"],["dc.contributor.author","Wolf, Joachim"],["dc.contributor.author","Schneider, Ilka"],["dc.contributor.author","Hermann, Andreas"],["dc.contributor.author","Metelmann, Moritz"],["dc.contributor.author","Kohl, Zacharias"],["dc.contributor.author","Linker, Ralf A."],["dc.contributor.author","Koch, Jan Christoph"],["dc.contributor.author","Büchner, Boriana"],["dc.contributor.author","Weiland, Ulrike"],["dc.contributor.author","Schönfelder, Erik"],["dc.contributor.author","Heinrich, Felix"],["dc.contributor.author","Osmanovic, Alma"],["dc.contributor.author","Klopstock, Thomas"],["dc.contributor.author","Dorst, Johannes"],["dc.contributor.author","Ludolph, Albert C."],["dc.contributor.author","Boentert, Matthias"],["dc.contributor.author","Hagenacker, Tim"],["dc.contributor.author","Deschauer, Marcus"],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Petri, Susanne"],["dc.contributor.author","Schreiber-Katz, Olivia"],["dc.date.accessioned","2021-04-14T08:27:57Z"],["dc.date.available","2021-04-14T08:27:57Z"],["dc.date.issued","2021"],["dc.date.updated","2022-02-09T13:21:17Z"],["dc.description.sponsorship","German Neuromuscular Society “Deutsche Gesellschaft fuer Muskelkranke\" e.V."],["dc.identifier.doi","10.3390/brainsci11030372"],["dc.identifier.eissn","2076-3425"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82457"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.publisher","MDPI"],["dc.relation.eissn","2076-3425"],["dc.rights","https://creativecommons.org/licenses/by/4.0/"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","A Nation-Wide, Multi-Center Study on the Quality of Life of ALS Patients in Germany"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]