Martin E. Schwab

ORCID: 0000-0001-6206-6150
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About
Contact & Profiles
Research Areas
  • Nerve injury and regeneration
  • Neurogenesis and neuroplasticity mechanisms
  • Axon Guidance and Neuronal Signaling
  • Spinal Cord Injury Research
  • Signaling Pathways in Disease
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Transcranial Magnetic Stimulation Studies
  • Neuroscience and Neuropharmacology Research
  • Nerve Injury and Rehabilitation
  • Neuropeptides and Animal Physiology
  • Stroke Rehabilitation and Recovery
  • Angiogenesis and VEGF in Cancer
  • Botulinum Toxin and Related Neurological Disorders
  • Urinary Bladder and Prostate Research
  • Retinal Development and Disorders
  • Spinal Dysraphism and Malformations
  • Cellular transport and secretion
  • Pain Mechanisms and Treatments
  • Toxin Mechanisms and Immunotoxins
  • Hereditary Neurological Disorders
  • Multiple Sclerosis Research Studies
  • Muscle activation and electromyography studies
  • Neurological disorders and treatments
  • Zebrafish Biomedical Research Applications
  • Traumatic Brain Injury and Neurovascular Disturbances

University of Zurich
2015-2024

ETH Zurich
2015-2024

Swiss Institute for Regenerative Medicine
2020-2023

Department of Medical Sciences
2012-2022

Anstalt für Verbrennungskraftmaschinen List (Austria)
2020

Board of the Swiss Federal Institutes of Technology
2019

TU Wien
2016-2018

Universitätsklinik Balgrist
2010-2015

Montanuniversität Leoben
2014-2015

École Polytechnique Fédérale de Lausanne
2003-2014

Lack of neurite growth in optic nerve explants vitro has been suggested to be due nonpermissive substrate properties higher vertebrate central nervous system (CNS) white matter. We have searched for surface components CNS matter, which would prevent growth. CNS, but not peripheral (PNS) myelin fractions from rat and chick were highly substrates vitro. used an spreading assay with 3T3 cells quantify qualities membrane isolated proteins reconstituted artificial lipid vesicles....

10.1083/jcb.106.4.1281 article EN The Journal of Cell Biology 1988-04-01

Abstract Local spinal cord lesions are often greatly enlarged by secondary damage, a process which leads to massive additional cell death. This is poorly understood. In order investigate types of cells could play role in increasing the size lesion, we have analysed events occurring at rat lesion sites from 1 h 3 months after partial transection using type‐specific markers. One hour transection, site was small and corresponded zone primary mechanical damage. Extravasation blood an opening –...

10.1111/j.1460-9568.1994.tb00983.x article EN European Journal of Neuroscience 1994-05-01

Brain-derived neurotrophic factor (BDNF) is a small, basic protein purified from the mammalian brain that has been shown previously to support survival of cultured spinal sensory neurons (Barde et al., 1982). In current studies, BDNF was tested for its ability CNS cells isolated perinatal rat retina. Both immunofluorescent labeling Thy-1 and prior retrograde with HRP were used as retinal ganglion cell markers in vitro. With embryonic day (E) 17 retinas, it found allowed small subpopulation...

10.1523/jneurosci.06-10-03031.1986 article EN cc-by-nc-sa Journal of Neuroscience 1986-10-01

Numerous obstacles to successful regeneration of injured axons in the adult mammalian spinal cord exist. Consequently, a treatment strategy inducing axonal and significant functional recovery after injury has overcome these obstacles. The current study attempted address multiple impediments by using combinatory complete transection rats: (1) reduce inhibitory cues glial scar (chondroitinase ABC), (2) provide growth-supportive substrate for [Schwann cells (SCs)], (3) enable regenerated exit...

10.1523/jneurosci.3562-04.2005 article EN cc-by-nc-sa Journal of Neuroscience 2005-02-02

Nogo-A is a neurite growth inhibitor involved in regenerative failure and restriction of structural plasticity the adult CNS. Three major protein products (Nogo-A, -B, -C) are derived from the<i>nogo</i> gene. Here we describe embryonic postnatal expression three Nogo isoforms rat by <i>in situ</i> hybridization immunohistochemistry. Northern Western blot analysis indicated that predominantly expressed nervous system with lower levels also present testis heart. In CNS myelin, confocal...

10.1523/jneurosci.22-09-03553.2002 article EN Journal of Neuroscience 2002-05-01

Nogo-A is a potent neurite growth inhibitor in vitro and plays role both the restriction of axonal regeneration after injury structural plasticity CNS higher vertebrates. The regions that mediate inhibition topology molecule plasma membrane have to be defined. Here we demonstrate presence three different active sites: (1) an N-terminal region involved fibroblast spreading, (2) stretch encoded by Nogo-A-specific exon restricts outgrowth cell spreading induces cone collapse, (3) C-terminal...

10.1523/jneurosci.23-13-05393.2003 article EN Journal of Neuroscience 2003-07-02

Abstract Lesion‐induced inflammatory responses in both brain and spinal cord have recently become a topic of active investigation. Using C57BL/6J mice, we compared the tissue reaction these two central nervous system (CNS) compartments with mechanical lesions similar size involving grey white matter. This evaluation included quantitative assessment neutrophils, lymphocytes activated macrophages/microglia, as well astrocyte activation, upregulation vascular cell adhesion molecules (ICAM‐1,...

10.1046/j.1460-9568.1999.00792.x article EN European Journal of Neuroscience 1999-10-01

Abstract Spinal cord trauma leads to loss of motor, sensory and autonomic functions below the lesion. Recovery is very restricted, due in part neurite growth inhibitory myelin proteins, particular Nogo‐A. Two neutralizing antibodies against Nogo‐A were used study recovery axonal regeneration after spinal lesions. Three months old Lewis rats tested sensory‐motor tasks (open field locomotion, crossing ladder rungs narrow beams, CatWalk® runway, reactions heat von Frey hairs). A T‐shaped lesion...

10.1002/ana.20627 article EN Annals of Neurology 2005-09-19
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