The neuropathological basis of clinical progression in multiple sclerosis. - Wikidata - awgldk - TriplyDB

The neuropathological basis of clinical progression in multiple sclerosis.

The neuropathological basis of clinical progression in multiple sclerosis.

http://www.wikidata.org/entity/Q34188436

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Exploring potential mechanisms of action of natalizumab in secondary progressive multiple sclerosis Intrathecal IgG synthesis: a resistant and valuable target for future multiple sclerosis treatments Common transcriptional signatures in brain tissue from patients with HIV-associated neurocognitive disorders, Alzheimer's disease, and Multiple Sclerosis Phosphodiesterases in neurodegenerative disorders A Personalized Approach in Progressive Multiple Sclerosis: The Current Status of Disease Modifying Therapies (DMTs) and Future Perspectives A gradient in cortical pathology in multiple sclerosis by in vivo quantitative 7 T imaging Feasibility of the use of combinatorial chemokine arrays to study blood and CSF in multiple sclerosis Free serum haemoglobin is associated with brain atrophy in secondary progressive multiple sclerosis Clinical, MRI, and CSF markers of disability progression in multiple sclerosis.The role of the cerebellum in multiple sclerosis.The Relationship between Gray Matter Quantitative MRI and Disability in Secondary Progressive Multiple Sclerosis Patient-reported outcomes and survival in multiple sclerosis: A 10-year retrospective cohort study using the Multiple Sclerosis Impact Scale-29.Meningeal inflammation plays a role in the pathology of primary progressive multiple sclerosis.Extensive grey matter pathology in the cerebellum in multiple sclerosis is linked to inflammation in the subarachnoid space.An updated histological classification system for multiple sclerosis lesions.Histamine H(3) receptor integrates peripheral inflammatory signals in the neurogenic control of immune responses and autoimmune disease susceptibility Neurofascin 140 is an embryonic neuronal neurofascin isoform that promotes the assembly of the node of Ranvier Tissue transglutaminase in marmoset experimental multiple sclerosis: discrepancy between white and grey matter.Total-tau in cerebrospinal fluid of patients with multiple sclerosis decreases in secondary progressive stage of disease and reflects degree of brain atrophy.Neuronal activity regulates remyelination via glutamate signalling to oligodendrocyte progenitors Pharmacological Approaches to the Management of Secondary Progressive Multiple Sclerosis.Targeted inhibition of complement using complement receptor 2-conjugated inhibitors attenuates EAE.Increased HLA-E expression in white matter lesions in multiple sclerosis.Elevated immune-inflammatory signaling in mood disorders: a new therapeutic target?Current and emerging therapies for the treatment of multiple sclerosis: focus on cladribine.Origins and significance of astrogliosis in the multiple sclerosis model, MOG peptide EAE Complement is activated in progressive multiple sclerosis cortical grey matter lesions.Progressive Dwindling in Multiple Sclerosis: An Opportunity to Improve Care Dynamic imaging of individual remyelination profiles in multiple sclerosis.Modeling the Chronic Loss of Optic Nerve Axons and the Effects on the Retinal Nerve Fiber Layer Structure in Primary Disorder of Myelin.Cerebellar abnormalities contribute to disability including cognitive impairment in multiple sclerosis.Onset of secondary progressive MS after long-term rituximab therapy - a case report.Molecular recognition theory and sense-antisense interaction: therapeutic applications in autoimmunity Polymorphism in Leptin and Leptin Receptor Genes May Modify Leptin Levels and Represent Risk Factors for Multiple Sclerosis.Secondary Progressive Multiple Sclerosis: Definition and Measurement.Neuronal loss, demyelination and volume change in the multiple sclerosis neocortex.Tissue microarray methodology identifies complement pathway activation and dysregulation in progressive multiple sclerosis.Anti-CD20 inhibits T cell-mediated pathology and microgliosis in the rat brain.The influence of HLA-DRB1*15 on motor cortical pathology in multiple sclerosis.Tumor necrosis factor is elevated in progressive multiple sclerosis and causes excitotoxic neurodegeneration.

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P2860

The neuropathological basis of clinical progression in multiple sclerosis.

http://www.wikidata.org/entity/Q34188436

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2011 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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name

The neuropathological basis of clinical progression in multiple sclerosis.

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The neuropathological basis of clinical progression in multiple sclerosis.

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The neuropathological basis of clinical progression in multiple sclerosis.

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type

label

The neuropathological basis of clinical progression in multiple sclerosis.

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The neuropathological basis of clinical progression in multiple sclerosis.

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The neuropathological basis of clinical progression in multiple sclerosis.

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prefLabel

The neuropathological basis of clinical progression in multiple sclerosis.

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The neuropathological basis of clinical progression in multiple sclerosis.

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The neuropathological basis of clinical progression in multiple sclerosis.

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The neuropathological basis of clinical progression in multiple sclerosis.

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Bishan Radotra

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Djordje Gveric

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Federico Roncaroli

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Owain Howell

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Richard Nicholas

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P2860

Detection of cortical inflammatory lesions by double inversion recovery magnetic resonance imaging in patients with multiple sclerosis

Relapsing and remitting multiple sclerosis: pathology of the newly forming lesion

Intracortical lesions in multiple sclerosis: improved detection with 3D double inversion-recovery MR imaging

Homogeneity of active demyelinating lesions in established multiple sclerosis

Gray matter involvement in multiple sclerosis

Compartmentalization of inflammation in the CNS: a major mechanism driving progressive multiple sclerosis

Regional variations in the extent and pattern of grey matter demyelination in multiple sclerosis: a comparison between the cerebral cortex, cerebellar cortex, deep grey matter nuclei and the spinal cord

Multiple sclerosis

Heterogeneity of multiple sclerosis lesions: implications for the pathogenesis of demyelination

Axonal transection in the lesions of multiple sclerosis

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