A5044468051- Neurogenesis and neuroplasticity mechanisms
- Multiple Sclerosis Research Studies
- Neuroinflammation and Neurodegeneration Mechanisms
- Peripheral Neuropathies and Disorders
- Nerve injury and regeneration
- Hereditary Neurological Disorders
- Neuroscience and Neuropharmacology Research
- Glycosylation and Glycoproteins Research
- RNA Research and Splicing
- RNA regulation and disease
- MicroRNA in disease regulation
- Axon Guidance and Neuronal Signaling
- Alzheimer's disease research and treatments
- Signaling Pathways in Disease
- Anesthesia and Neurotoxicity Research
- Cytokine Signaling Pathways and Interactions
- Neurological diseases and metabolism
- Mitochondrial Function and Pathology
- Galectins and Cancer Biology
- Amyotrophic Lateral Sclerosis Research
- Cell Adhesion Molecules Research
- Skin and Cellular Biology Research
- Cellular Mechanics and Interactions
- Systemic Lupus Erythematosus Research
- Polyomavirus and related diseases
Cleveland Clinic Lerner College of Medicine
2016-2025
Cleveland Clinic
2012-2024
Case Western Reserve University
1998-2024
University School
1998-2024
Cerner (United States)
2020
Multiple Sclerosis Research Institute
2020
Center for Neurosciences
2019
Neurosciences Institute
1998-2014
University Medical Center
2014
Montreal Neurological Institute and Hospital
2001-2012
Multiple sclerosis is an inflammatory demyelinating disease of the central nervous system and most common cause neurologic disability in young adults. Despite antiinflammatory or immunosuppressive therapy, patients have progressive deterioration that may reflect axonal loss. We conducted pathological studies brain tissues to define changes axons with multiple sclerosis.
Multiple Sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system that causes motor, sensory, and cognitive deficits. The present study characterized demyelinated lesions in cerebral cortex MS patients. One hundred twelve cortical were identified 110 tissue blocks from 50 Three patterns demyelination identified: Type I contiguous with subcortical white matter lesions; II small, confined to cortex, often perivascular; III extended pial surface layer 3 or 4....
Multiple sclerosis is an inflammatory disease of the central nervous system that destroys myelin, oligodendrocytes, and axons. Since most lesions multiple are not remyelinated, enhancement remyelination a possible therapeutic strategy could perhaps be achieved with transplantation oligodendrocyte-producing cells into lesions. We investigated frequency distribution configuration oligodendrocytes in chronic to determine whether these factors limit remyelination.
Abstract Objective Degeneration of chronically demyelinated axons is a major cause irreversible neurological disability in multiple sclerosis (MS) patients. Development neuroprotective therapies will require elucidation the molecular mechanisms by which neurons and degenerate. Methods We report ultrastructural changes that support Ca2+‐mediated destruction MS compared expression levels 33,000 characterized genes postmortem motor cortex from six control brains matched for age, sex, interval....
The extent and pattern of demyelination in the cerebral cortex was determined 78 tissue blocks from brains 20 multiple sclerosis (MS) patients 28 7 without neurological disease. Tissue 4 predetermined areas (cingulate gyrus, frontal, parietal, temporal lobe) were studied, irrespective macroscopically evident MS plaques. All contained periventricular and/or subcortical white matter. One hundred nine demyelinating lesions detected cortex, which 92 (84.4%) purely intracortical 17 (15.6%)...
Multiple sclerosis (MS) is characterized by multifocal loss of myelin, oligodendrocytes, and axons. Potential MS therapies include enhancement remyelination transplantation or manipulation endogenous oligodendrocyte progenitor cells. Characteristics progenitors in normal human brain lesions have not been studied extensively. This report describes the distribution cells sections from adult using antibodies directed against NG2, an integral membrane chondroitin sulfate proteoglycan expressed...
Abstract The amount of messenger RNA encoding human inducible nitric oxide synthase and the presence distribution NADPH diaphorase were determined in tissue sections from multiple sclerosis (MS) control brains. Levels markedly elevated MS brains when compared to normal activity, a histochemical stain reflecting catalytic was detected reactive astrocytes active demyelinating lesions at edge chronic lesions. Control did not contain diaphorase–positive astrocytes. These results implicate free...
Axonal degeneration has been proposed as a cause of irreversible neurological disability in multiple sclerosis (MS) patients. The purpose this study was to quantify axonal loss spinal cord lesions from 5 paralyzed (Expanded Disability Status Scale score > or =7.5) MS patients and determine if number volume correlated with levels the neuronal marker N-acetyl aspartate (NAA). ranged 45 84% averaged 68%. NAA were significantly reduced (>50%) cross sections cords containing lesions. Reduced...
Fragile X-associated tremor/ataxia syndrome (FXTAS) is an adult-onset neurodegenerative disorder that affects carriers, principally males, of premutation alleles (55–200 CGG repeats) the fragile X mental retardation 1 (FMR1) gene. Clinical features FXTAS include progressive intention tremor and gait ataxia, accompanied by characteristic white matter abnormalities on MRI. The neuropathological hallmark intranuclear inclusion, present in both neurons astrocytes throughout CNS. Prior to current...
Myelination increases neuronal conduction velocity through its insulating properties and an unidentified extrinsic effect that axonal caliber. Although it is well established demyelination can cause atrophy, the myelin molecule regulates caliber not known. Loss of structural proteins compact peripheral nervous system (PNS) myelin, P0 protein, basic protein does lead to atrophy. This study demonstrates mice with a null mutation myelin-associated glycoprotein (MAG) gene have chronic atrophy...
The present study examined the extent and distribution of lymphocyte infiltration in demyelinated lesions cerebral cortex multiple sclerosis (MS) patients. Tissue sections from brain 10 MS patients five without neurological disease were double labeled for myelin basic protein markers C D3, D4, D8, D45RO, D20. highest density D3- positive T cells was found white matter (40.4/10 high power fields (hpf)). Fewer detected cortical that extended through both gray (12.1/10 hpf; P B-0.001). lowest...
Multiple sclerosis (MS), a common neurodegenerative disease of the CNS, is characterized by loss oligodendrocytes and demyelination. Tumor necrosis factor α (TNF-α), proinflammatory cytokine implicated in MS, can activate necroptosis, necrotic cell death pathway regulated RIPK1 RIPK3 under caspase-8-deficient conditions. Here, we demonstrate defective caspase-8 activation, as well activation RIPK1, RIPK3, MLKL, hallmark mediators cortical lesions human MS pathological samples. Furthermore,...