Pathogenesis of axonal and neuronal damage in multiple sclerosis

No abstract is available for this paper.

• Publication year

  2007

• Venue

  Neurology

• Publication date

  2007-05-29

• Fields of study

  Medicine

• Identifiers
  DOI 10.1212/01.wnl.0000275229.13012.32PMID 17548565
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Neurology®

  2007cited by this paper
• Multiple Sclerosis

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• Evidence for synaptic stripping by cortical microglia

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• MULTIPLE SCLEROSIS AS A NEURONAL DISEASE

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• Mitochondrial dysfunction as a cause of axonal degeneration in multiple sclerosis patients

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• Evolution of a neuroprotective function of central nervous system myelin

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• Multiple sclerosis as a neuronal disease.

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• Microglia and neuroprotection: implications for Alzheimer's disease.

  2005cited by this paper
• Nuclear Ca2+ and the cAMP Response Element-Binding Protein Family Mediate a Late Phase of Activity-Dependent Neuroprotection

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• Axonal degeneration in multiple sclerosis: Is it time for neuroprotective strategies?

  2004cited by this paper
• White matter injury mechanisms.

  2004cited by this paper
• Displacement of synaptic terminals from regenerating motoneurons by microglial cells

  2004cited by this paper
• Multiple sclerosis: brain-infiltrating CD8+ T cells persist as clonal expansions in the cerebrospinal fluid and blood.

  2004cited by this paper
• Co-localization of sodium channel Nav1.6 and the sodium-calcium exchanger at sites of axonal injury in the spinal cord in EAE.

  2004cited by this paper
• Synaptic stripping in the human facial nucleus

  2004cited by this paper
• Na+ channel expression along axons in multiple sclerosis and its models.

  2004cited by this paper
• Molecular changes in neurons in multiple sclerosis: altered axonal expression of Nav1.2 and Nav1.6 sodium channels and Na+/Ca2+ exchanger.

  2004cited by this paper
• Axonal protection using flecainide in experimental autoimmune encephalomyelitis

  2004cited by this paper
• Sodium channel blockade with phenytoin protects spinal cord axons, enhances axonal conduction, and improves functional motor recovery after contusion SCI.

  2004cited by this paper
• Subpial Demyelination in the Cerebral Cortex of Multiple Sclerosis Patients

  2003cited by this paper
• Vulnerability of Human Neurons to T Cell-Mediated Cytotoxicity1

  2003cited by this paper
• Evidence for axonal pathology and adaptive cortical reorganization in patients at presentation with clinically isolated syndromes suggestive of multiple sclerosis

  2003cited by this paper
• Axonal loss in the pathology of MS: consequences for understanding the progressive phase of the disease.

  2003cited by this paper
• Disruption of Cnp1 uncouples oligodendroglial functions in axonal support and myelination

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• Imaging neuronal and axonal degeneration in multiple sclerosis

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• Inflammation and degeneration in multiple sclerosis

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• Blockers of sodium and calcium entry protect axons from nitric oxide‐mediated degeneration

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• Abnormal sodium channel distribution in optic nerve axons in a model of inflammatory demyelination.

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• Potentially adaptive functional changes in cognitive processing for patients with multiple sclerosis and their acute modulation by rivastigmine.

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• The Yin and Yang of NMDA receptor signalling.

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• Altered expression patterns of group I and II metabotropic glutamate receptors in multiple sclerosis.

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• Intracortical multiple sclerosis lesions are not associated with increased lymphocyte infiltration

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• Why did NMDA receptor antagonists fail clinical trials for stroke and traumatic brain injury?

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• Acute axonal damage in multiple sclerosis is most extensive in early disease stages and decreases over time.

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• Is Gadolinium Enhancement Predictive of the Development of Brain Atrophy in Multiple Sclerosis? A Review of the Literature

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• The role of nitric oxide in multiple sclerosis.

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• Cortical motor reorganization after a single clinical attack of multiple sclerosis.

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• Measurement of atrophy in multiple sclerosis: pathological basis, methodological aspects and clinical relevance.

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• Axonal loss in normal-appearing white matter in a patient with acute MS

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• Axonal Loss in Multiple Sclerosis

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• Multiple sclerosis: a white matter disease with associated gray matter damage

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• A Pathogenic Role for Myelin-Specific Cd8+ T Cells in a Model for Multiple Sclerosis

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• Transected neurites, apoptotic neurons, and reduced inflammation in cortical multiple sclerosis lesions

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• Distribution of a calcium channel subunit in dystrophic axons in multiple sclerosis and experimental autoimmune encephalomyelitis.

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• Multiple sclerosis: Altered glutamate homeostasis in lesions correlates with oligodendrocyte and axonal damage

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• Transection of major histocompatibility complex class I-induced neurites by cytotoxic T lymphocytes.

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• CNS energy metabolism as related to function.

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• Clonal Expansions of Cd8+ T Cells Dominate the T Cell Infiltrate in Active Multiple Sclerosis Lesions as Shown by Micromanipulation and Single Cell Polymerase Chain Reaction

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• Multiple sclerosis.

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• Axonal changes in chronic demyelinated cervical spinal cord plaques.

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• Evidence for adaptive functional changes in the cerebral cortex with axonal injury from multiple sclerosis.

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• Important role of reverse Na(+)-Ca(2+) exchange in spinal cord white matter injury at physiological temperature.

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• Cortical cerebral metabolism correlates with MRI lesion load and cognitive dysfunction in MS

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• Total brain N-acetylaspartate

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• Remyelinating the demyelinated CNS.

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• Oxidative damage to mitochondrial DNA and activity of mitochondrial enzymes in chronic active lesions of multiple sclerosis.

  2000cited by this paper
• Neurological disability correlates with spinal cord axonal loss and reduced N‐acetyl aspartate in chronic multiple sclerosis patients

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• Catch-Up Growth in Short-at-Birth NICU Graduates

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• The neuropathology of multiple sclerosis.

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• Axonal pathology in multiple sclerosis: relationship to neurologic disability.

  1999cited by this paper
• Spinal cord axonal loss in multiple sclerosis: a post‐mortem study

  1999cited by this paper
• Axonal pathology in demyelinating diseases

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• Axonal pathology in myelin disorders

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• A longitudinal study of brain atrophy in relapsing multiple sclerosis

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• Axonal Pathology in Multiple Sclerosis. A Historical Note

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• Magnetic resonance spectroscopy: imaging axonal damage in MS.

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• Integrating innate and adaptive immunity in the whole animal

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• Microglia as mediators of inflammatory and degenerative diseases.

  1999cited by this paper
• The natural history of multiple sclerosis: a geographically based study. 5. The clinical features and natural history of primary progressive multiple sclerosis.

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• Use of the brain parenchymal fraction to measure whole brain atrophy in relapsing-remitting MS

  1999cited by this paper
• Magnetic resonance imaging in the monitoring of disease progression in multiple sclerosis

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• Reactive microgliosis.

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• Cortical lesions in multiple sclerosis.

  1999cited by this paper
• Neurodegeneration in Multiple Sclerosis: Relationship to Neurological Disability

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• Axonal swellings and degeneration in mice lacking the major proteolipid of myelin.

  1998cited by this paper
• Axonal damage correlates with disability in patients with relapsing-remitting multiple sclerosis. Results of a longitudinal magnetic resonance spectroscopy study.

  1998cited by this paper
• AXONAL TRANSECTION IN THE LESIONS OF MULTIPLE SCLEROSIS

  1998cited by this paper
• Myelin-Associated Glycoprotein Is a Myelin Signal that Modulates the Caliber of Myelinated Axons

  1998cited by this paper
• Measures of brain and spinal cord atrophy in multiple sclerosis.

  1998cited by this paper
• Neurofilament protein in cerebrospinal fluid: a potential marker of activity in multiple sclerosis

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• Putting Magnetic Resonance Spectroscopy Studies in Context: Axonal Damage and Disability in Multiple Sclerosis

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• Axonal transection in the lesions of multiple sclerosis.

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• Human autoimmune neuropathies.

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• Epidemiology of multiple sclerosis.

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• Inflammation in the nervous system.

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• Induction of nitric oxide synthase in demyelinating regions of multiple sclerosis brains

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• Brain macrophages: neurotoxic or neurotrophic effector cells?

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• Myelination in the absence of myelin-associated glycoprotein

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• Ionic mechanisms of anoxic injury in mammalian CNS white matter: role of Na+ channels and Na(+)-Ca2+ exchanger

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