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Journal Article
Journal of Neuroscience, ISSN 0270-6474, 06/2012, Volume 32, Issue 26, pp. 8855 - 8864
Journal Article
Glia, ISSN 0894-1491, 01/2016, Volume 64, Issue 1, pp. 155 - 174
Protein zero (P0) is the major structural component of peripheral myelin. Lack of this adhesion protein from Schwann cells causes a severe dysmyelinating... 
glia‐axonal support | myelin | Schwann cell | Dejerine‐Sottas syndrome | oligodendrocyte | neurodegeneration | neuropathy | Charcot‐Marie‐tooth disease | hereditary spastic paraplegia (SPG‐2) | Dejerine-Sottas syndrome | Oligodendrocyte | Myelin | Neurodegeneration | Charcot-Marie-tooth disease | Glia-axonal support | Neuropathy | Hereditary spastic paraplegia (SPG-2) | MARIE-TOOTH-DISEASE | COLONY-STIMULATING FACTOR | glia-axonal support | MAJOR STRUCTURAL PROTEIN | NEUROSCIENCES | MICE HETEROZYGOUSLY DEFICIENT | hereditary spastic paraplegia (SPG-2) | MOUSE MODEL | PELIZAEUS-MERZBACHER-DISEASE | CENTRAL-NERVOUS-SYSTEM | SCHWANN-CELL DEVELOPMENT | BASIC-PROTEIN | INHERITED DEMYELINATING NEUROPATHIES | Motor Activity - physiology | Optic Nerve - pathology | Phrenic Nerve - pathology | Myelin-Associated Glycoprotein - metabolism | Myelin Sheath - metabolism | Brain - metabolism | Sciatic Nerve - metabolism | Myelin Proteolipid Protein - metabolism | Female | Phrenic Nerve - metabolism | Myelin Sheath - pathology | Sciatic Nerve - pathology | Mice, Inbred C57BL | Kaplan-Meier Estimate | Axons - metabolism | Neural Conduction - physiology | Mice, Knockout | Mortality, Premature | Animals | Myelin Proteolipid Protein - genetics | Axons - pathology | Brain - pathology | Myelin P0 Protein - genetics | Myelin P0 Protein - metabolism | Optic Nerve - metabolism | Analysis | Myelin proteins | Proteins | Preservation | Rodents
Journal Article
Science, ISSN 0036-8075, 2/2008, Volume 319, Issue 5867, pp. 1244 - 1247
Journal Article
Journal Article
Glia, ISSN 0894-1491, 03/2014, Volume 62, Issue 3, pp. 387 - 398
The origin of α‐synuclein (α‐syn)‐positive glial cytoplasmic inclusions found in oligodendrocytes in multiple system atrophy (MSA) is enigmatic, given the fact... 
prion‐like transfer | glial cytoplasmic inclusion | multiple system atrophy | Glial cytoplasmic inclusion | Multiple system atrophy | Prion-like transfer | CELLS | INCLUSIONS | prion-like transfer | PATHOLOGY | MODEL | ENDOCYTOSIS | NEUROSCIENCES | NEURODEGENERATIVE-DISEASES | MICE | BRAIN | PARKINSONS-DISEASE | Embryo, Mammalian | Humans | Male | Dose-Response Relationship, Drug | Oligodendroglia - physiology | Basic Helix-Loop-Helix Transcription Factors - metabolism | Myelin Proteolipid Protein - metabolism | Neurons - physiology | Adenoviridae - genetics | Female | alpha-Synuclein - genetics | Brain - cytology | Receptor, Platelet-Derived Growth Factor alpha - metabolism | Transduction, Genetic | Mice, Inbred C57BL | Cells, Cultured | Rats | Oligodendrocyte Transcription Factor 2 | 2',3'-Cyclic-Nucleotide Phosphodiesterases - metabolism | Rats, Sprague-Dawley | Hydrazones - pharmacology | Nerve Tissue Proteins - metabolism | Animals | Mice | alpha-Synuclein - metabolism | Galactosylceramidase - metabolism | Oligomers | Proteins | RNA | Neurons | Analysis | Medical research | Pathogenesis | Animal models | Brain | Adenoviridae | Neurons and Cognition | Neurobiology | Life Sciences | Galactosylceramidase | Basic Helix-Loop-Helix Transcription Factors | Myelin Proteolipid Protein | 2',3'-Cyclic-Nucleotide Phosphodiesterases | Psychology and behavior | Hydrazones | Nerve Tissue Proteins | Receptor, Platelet-Derived Growth Factor alpha | Oligodendroglia | Cognitive Sciences | alpha-Synuclein | Basic Medicine | Neurosciences | Medical and Health Sciences | Medicin och hälsovetenskap | Medicinska och farmaceutiska grundvetenskaper | Neurovetenskaper
Journal Article
International Immunology, ISSN 0953-8178, 2011, Volume 23, Issue 9, pp. 565 - 573
Journal Article
Brain Pathology, ISSN 1015-6305, 09/2018, Volume 28, Issue 5, pp. 611 - 630
Pelizaeus‐Merzbacher disease (PMD) is a fatal hypomyelinating disorder characterized by early impairment of motor development, nystagmus, choreoathetotic... 
bioenergetic failure | antioxidants | oxidative stress | Pelizaeus‐Merzbacher disease | mitochondrial dynamics | Pelizaeus-Merzbacher disease | EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS | ALZHEIMERS-DISEASE | PATHOLOGY | PROTEOMIC IDENTIFICATION | NEUROSCIENCES | CLINICAL NEUROLOGY | AXONAL DEGENERATION | X-ADRENOLEUKODYSTROPHY | MULTIPLE-SCLEROSIS | CENTRAL-NERVOUS-SYSTEM | TRANSGENIC MOUSE MODEL | ENERGY-METABOLISM | MYELIN PROTEOLIPID PROTEIN | Mitochondrial Dynamics | Pelizaeus-Merzbacher Disease - metabolism | Spinal Cord - metabolism | Oxidative Stress | Humans | Child, Preschool | DNA, Mitochondrial | Infant | Male | RNA, Messenger - metabolism | Mitochondrial Proteins - metabolism | Pelizaeus-Merzbacher Disease - pathology | Spinal Cord - pathology | Myelin Proteolipid Protein - metabolism | Child | Fibroblasts - metabolism | Mice, Inbred C57BL | Cells, Cultured | Mice, Transgenic | Mitochondria - metabolism | Mitochondria - pathology | Fibroblasts - pathology | Animals | Myelin Proteolipid Protein - genetics | Glutamic Acid - metabolism | Antioxidants | Oxidative stress | Enzymes | Cysteine | Creatine kinase | Analysis | Mitochondrial DNA | Creatine | Myelin proteins | Tricarboxylic acid cycle | Phosphorylation | Reactive oxygen species | Central nervous system | Impairment | Homeostasis | Motors | Krebs cycle | Depolarization | Proteins | Cords | Mitochondria | Myelin proteolipid protein | Neurodegeneration | Oligodendrocytes | Fibroblasts | Ataxia | Phenotypes | Myelin | Abnormalities | Spasticity | Pharmacology | Life span | Oxidative phosphorylation | Morphology | Proteolipid protein | Nystagmus | Glycolysis | Life Sciences
Journal Article