Patients lacking the major CNS myelin protein, proteolipid protein 1, develop length-dependent axonal degeneration in the absence of demyelination and inflammation. - Wikidata - wikimedia - TriplyDB

Patients lacking the major CNS myelin protein, proteolipid protein 1, develop length-dependent axonal degeneration in the absence of demyelination and inflammation.

Patients lacking the major CNS myelin protein, proteolipid protein 1, develop length-dependent axonal degeneration in the absence of demyelination and inflammation.

http://www.wikidata.org/entity/Q43901506

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Alzheimer's disease as homeostatic responses to age-related myelin breakdown Myelin damage and repair in pathologic CNS: challenges and prospects Hypomyelinating leukodystrophies: translational research progress and prospects Pelizaeus-Merzbacher disease and spastic paraplegia type 2: two faces of myelin loss from mutations in the same gene Myelin-mediated inhibition of oligodendrocyte precursor differentiation can be overcome by pharmacological modulation of Fyn-RhoA and protein kinase C signalling Oligodendrocytes: biology and pathology HEREDITARY MYELOPATHIES.Lamin B1 mediates cell-autonomous neuropathology in a leukodystrophy mouse model.Diffusion tensor MRI as a biomarker in axonal and myelin damage.Diffusion tensor imaging of patients with proteolipid protein 1 gene mutations.Heterogeneity in oligodendroglia: Is it relevant to mouse models and human disease?Myelin loss does not lead to axonal degeneration in a long-lived model of chronic demyelination Oligodendroglia metabolically support axons and contribute to neurodegeneration.High-resolution diffusion tensor imaging of fixed brain in a mouse model of Pelizaeus-Merzbacher disease: comparison with quantitative measures of white matter pathology.Increased Plp1 gene expression leads to massive microglial cell activation and inflammation throughout the brain Axon-glial interaction in the CNS: what we have learned from mouse models of Pelizaeus-Merzbacher disease.Clinical spectrum of 4H leukodystrophy caused by POLR3A and POLR3B mutations.Using temporal genetic switches to synchronize the unfolded protein response in cell populations in vivo.A new mutation in GJC2 associated with subclinical leukodystrophy.The myelin mutants as models to study myelin repair in the leukodystrophies.Glia Disease and Repair-Remyelination Modeling the natural history of Pelizaeus-Merzbacher disease.Insertion of proteolipid protein into oligodendrocyte mitochondria regulates extracellular pH and adenosine triphosphate Evolution of a neuroprotective function of central nervous system myelin.Oligodendroglial modulation of fast axonal transport in a mouse model of hereditary spastic paraplegia.Quantifying the carrier female phenotype in Pelizaeus-Merzbacher disease.Myelin repair: the role of stem and precursor cells in multiple sclerosis Oligodendrocyte morphometry and expression of myelin - Related mRNA in ventral prefrontal white matter in major depressive disorder The molecular and cellular defects underlying Pelizaeus-Merzbacher disease.Protecting axons in multiple sclerosis.Effects of osmolality on PLP-null myelin structure: implications re axon damage.Neuronal loss in Pelizaeus-Merzbacher disease differs in various mutations of the proteolipid protein 1.Axon degeneration: Linking axonal bioenergetics to myelin.Axonal transport defects in neurodegenerative diseases.Concise Review: Stem Cell-Based Treatment of Pelizaeus-Merzbacher Disease.Neuroradiologic correlates of clinical disability and progression in the X-linked leukodystrophy Pelizaeus-Merzbacher disease Neuroprotection and repair in multiple sclerosis.Cuprizone-induced demyelination as a tool to study remyelination and axonal protection.Oligodendroglia: metabolic supporters of axons.Concepts for regulation of axon integrity by enwrapping glia.

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P2860

Patients lacking the major CNS myelin protein, proteolipid protein 1, develop length-dependent axonal degeneration in the absence of demyelination and inflammation.

http://www.wikidata.org/entity/Q43901506

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2002 nî lūn-bûn

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2002年学术文章

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Patients lacking the major CNS ...... emyelination and inflammation.

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Patients lacking the major CNS ...... emyelination and inflammation.

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Patients lacking the major CNS ...... emyelination and inflammation.

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Patients lacking the major CNS ...... emyelination and inflammation.

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Patients lacking the major CNS ...... emyelination and inflammation.

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Patients lacking the major CNS ...... emyelination and inflammation.

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Patients lacking the major CNS ...... demyelination and inflammation

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Donald A Yool

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Gregory J Moore

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Ian B Wilds

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Ian R Griffiths

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James Y Garbern

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John A Kamholz

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Klaus-Amin Nave

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Marjo S van der Knaap

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Matthias Klugmann

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Michael W Faulk

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P2860

The proteolipid protein gene and myelin disorders in man and animal models

Late-onset neurodegeneration in mice with increased dosage of the proteolipid protein gene

Axonal transection in the lesions of multiple sclerosis

Neurological dysfunction and axonal degeneration in Charcot-Marie-Tooth disease type 1A.

X-linked dominant hereditary motor and sensory neuropathy.

Axonal phenotype of Charcot-Marie-Tooth disease associated with a mutation in the myelin protein zero gene

Multisection proton MR spectroscopic imaging of the brain.

Isolation and characterization of autoreactive proteolipid protein-peptide specific T-cell clones from multiple sclerosis patients.

Regional age dependence of human brain metabolites from infancy to adulthood as detected by quantitative localized proton MRS.

Evidence for neuroaxonal injury in patients with proteolipid protein gene mutations.

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551-561

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10.1093/BRAIN/AWF043

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P433

Pt 3

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125

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Erik Sistermans

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2002-03-01T00:00:00Z

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11489186

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