A5071319008- Nerve injury and regeneration
- Neurogenesis and neuroplasticity mechanisms
- Traumatic Brain Injury and Neurovascular Disturbances
- Spinal Cord Injury Research
- Traumatic Brain Injury Research
- Axon Guidance and Neuronal Signaling
- S100 Proteins and Annexins
- Neonatal and fetal brain pathology
- Neuroinflammation and Neurodegeneration Mechanisms
- Neuroscience and Neuropharmacology Research
- Mitochondrial Function and Pathology
- Zebrafish Biomedical Research Applications
- EEG and Brain-Computer Interfaces
- Transcranial Magnetic Stimulation Studies
- Cardiac Arrest and Resuscitation
- Cell death mechanisms and regulation
- RNA Interference and Gene Delivery
- Anesthesia and Neurotoxicity Research
- Multiple Sclerosis Research Studies
- Functional Brain Connectivity Studies
- Metabolism and Genetic Disorders
- Noise Effects and Management
- interferon and immune responses
- Redox biology and oxidative stress
- Fetal and Pediatric Neurological Disorders
Ludwig-Maximilians-Universität München
2014-2025
Urologische Klinik München
2018-2025
Munich Cluster for Systems Neurology
2014-2025
LMU Klinikum
2018-2025
ETH Zurich
2002-2007
Harvard University
2004-2007
Harvard University Press
2005
University of Zurich
2002-2004
École Polytechnique Fédérale de Lausanne
2004
Washington University in St. Louis
2004
Object. Mild, traumatic repetitive head injury (RHI) leads to neurobehavioral impairment and is associated with the early onset of neurodegenerative disease. The authors developed an animal model investigate behavioral pathological changes RHI. Methods. Adult male C57BL/6 mice were subjected a single (43 mice), (two injuries 24 hours apart; 49 or no impact (36 mice). Cognitive function was assessed using Morris water maze test, neurological motor evaluated battery neuroscore, rotarod,...
In the peripheral nervous system (PNS), damaged axons regenerate successfully, whereas in CNS fail to regrow. neurons of dorsal root ganglia (DRG), which extend branches both PNS and CNS, only a lesion but not induces axonal growth. How this differential growth response is regulated vivo incompletely understood. Here, we combine time-lapse fluorescence microscopy with genetic manipulations mice reveal how transcription factor STAT3 regulates regeneration. We show that selective deletion DRG...
Nogo-A is a myelin-associated neurite outgrowth inhibitory protein limiting recovery and plasticity after central nervous system injury. In this study, purified monoclonal anti—Nogo-A antibody (7B12) was evaluated in two rat stroke models with time-to-treatment of 24 hours After photothrombotic cortical injury (PCI) intraventricular infusion control mouse immunoglobulin G for 2 weeks, long-term contralateral forepaw function reduced to about 55% prelesion performance until the latest time...
Lesion-induced plasticity of the rat corticospinal tract (CST) decreases postnatally, simultaneously with myelin appearance. In adult rats, compensatory sprouting can be induced by monoclonal antibody (mAb) IN-1 raised against growth inhibitory protein Nogo-A. this study, we examined separately fate sensory and motor fibers after mAb application. Intact rats treated exhibited an increase aberrant CST projections, i.e., projecting into ventral horn dorsally. Unilateral lesion [pyramidotomy...
Abstract Following lesion of the central nervous system (CNS), reinnervation denervated areas may occur via two distinct processes: regeneration lesioned fibres or/and sprouting from adjacent intact into deafferented zone. Both and axonal are very limited in fully mature CNS higher vertebrates, but can be enhanced by neutralizing neurite outgrowth inhibitory protein Nogo‐A. This study takes advantage spinal projection pattern descending tracts, corticospinal tract (CST) rubrospinal (RST), to...
In multiple sclerosis (MS), inflammation in the central nervous system (CNS) leads to damage of axons and myelin. Early during clinical course, patients can compensate this damage, but little is known about changes that underlie improvement neurological function. To study axonal may contribute recovery, we made use an animal model MS, which allows us target inflammatory lesions corticospinal tract (CST), a major descending motor pathway. We demonstrate remodel at levels response single...
The nuclear enzyme poly(ADP-ribose) polymerase (PARP), which has been shown to be activated following experimental traumatic brain injury (TBI), binds DNA strand breaks and utilizes nicotinamide adenine dinucleotide (NAD) as a substrate. Since consumption of NAD may deleterious recovery in the setting CNS injury, we examined effect potent PARP inhibitor, GPI 6150, on histological outcome TBI rat. Rats (n = 16) were anesthetized, received preinjury dose 6150 (30 min; 15 mg/kg, i.p.),...
Brain trauma is the main cause of morbidity and mortality in young adults. One delayed events that occurs after a head compromises survival patients cerebral edema. The present study examined first occurrence edema traumatic brain injury (TBI) induced by moderate fluid percussion rats. water content was measured from 1 h to 7 days posttrauma, hippocampus cortex, on both ipsi- contralateral hemispheres. Second, effects mannitol, an osmotic agent frequently used clinic, riluzole,...
Abstract In neuroscience research, the refined analysis of rodent locomotion is complex and cumbersome, access to technique limited because necessity for expensive equipment. this study, we implemented a new deep learning-based open-source toolbox Automated Limb Motion Analysis (ALMA) that requires only basic behavioral equipment an inexpensive camera. The ALMA enables consistent comprehensive analyses locomotor kinematics paw placement can be applied neurological conditions affecting brain...
Inflammation in the central nervous system can impair function of neuronal mitochondria and contributes to axon degeneration common neuroinflammatory disease multiple sclerosis (MS). Here we combine cell-type-specific mitochondrial proteomics with vivo biosensor imaging dissect how inflammation alters molecular composition functional capacity mitochondria. We show that lesions mouse spinal cord cause widespread persisting axonal ATP deficiency, which precedes oxidation calcium overload. This...
The neuroprotective effect of magnesium chloride (MgCl2), a compound previously demonstrated to improve behavioral and neurochemical outcome in several models experimental brain injury, was evaluated the present study. Male Sprague–Dawley rats were anesthetized subjected lateral fluid-percussion injury moderate severity (2.5–2.8 atm). A cannula implanted left femoral vein at 1 h following animals randomly received 15 min i.v. infusion either MgCl2 (125 μmol/rat) or saline. second group...
Large-conductance, calcium-activated potassium (maxi-K) channels regulate neurotransmitter release and neuronal excitability, openers of these have been shown to be neuroprotective in models cerebral ischemia. The authors evaluated the effects postinjury systemic administration maxi-K channel opener, BMS-204352, on behavioral histologic outcome after lateral fluid percussion (FP) traumatic brain injury (TBI) rat. Anesthetized Sprague-Dawley rats (n = 142) were subjected moderate FP 88) or...