Oligodendrocytes are integral to efficient neuronal signaling. Loss of myelinating oligodendrocytes is a central feature of many neurological diseases, including multiple sclerosis (MS). The results of neuropathological studies suggest that oligodendrocytes react with differing sensitivity to toxic insults, with some cells dying early during lesion development and some cells being resistant for weeks. This proposed graded vulnerability has never been demonstrated but provides an attractive window for therapeutic interventions. Furthermore, the biochemical pathways associated with graded oligodendrocyte vulnerability have not been well explored. We used immunohistochemistry and serial block-face scanning electron microscopy (3D-SEM) to show that cuprizone-induced metabolic stress results in an "out of phase" degeneration of oligodendrocytes. Although expression induction of stress response transcription factors in oligodendrocytes occurs within days, subsequent oligodendrocyte apoptosis continues for weeks. In line with the idea of an out of phase degeneration of oligodendrocytes, detailed ultrastructural reconstructions of the axon-myelin unit demonstrate demyelination of single internodes. In parallel, genome wide array analys...Continue Reading
The presence of malfolded proteins in the endoplasmic reticulum signals the induction of glucose-regulated proteins
Quantitative examination of internodal length of remyelinated nerve fibres in the central nervous system
The promoter region of the yeast KAR2 (BiP) gene contains a regulatory domain that responds to the presence of unfolded proteins in the endoplasmic reticulum.
Low glutathione and high iron govern the susceptibility of oligodendroglial precursors to oxidative stress
Microglial and astrocyte chemokines regulate monocyte migration through the blood-brain barrier in human immunodeficiency virus-1 encephalitis
Oligodendroglial modulation of fast axonal transport in a mouse model of hereditary spastic paraplegia
CHOP induces death by promoting protein synthesis and oxidation in the stressed endoplasmic reticulum
Increased expression of endoplasmic reticulum stress-related signaling pathway molecules in multiple sclerosis lesions
Selective regulation of growth factor expression in cultured cortical astrocytes by neuro-pathological toxins
Expression profiles of endoplasmic reticulum stress-related molecules in demyelinating lesions and multiple sclerosis
Chop (Ddit3) is essential for D469del-COMP retention and cell death in chondrocytes in an inducible transgenic mouse model of pseudoachondroplasia
Increased expression of ER stress- and hypoxia-associated molecules in grey matter lesions in multiple sclerosis
C/EBP homologous protein (CHOP) deficiency aggravates hippocampal cell apoptosis and impairs memory performance
Short-term cuprizone feeding induces selective amino acid deprivation with concomitant activation of an integrated stress response in oligodendrocytes
Impaired eukaryotic translation initiation factor 2B activity specifically in oligodendrocytes reproduces the pathology of vanishing white matter disease in mice
Short-term cuprizone feeding verifies N-acetylaspartate quantification as a marker of neurodegeneration
The sphingosine 1-phosphate receptor agonist FTY720 is neuroprotective after cuprizone-induced CNS demyelination
Tunicamycin-induced ER stress regulates chemokine CCL5 expression and secretion via STAT3 followed by decreased transmigration of MCF-7 breast cancer cells
Adult neural precursor cells from the subventricular zone contribute significantly to oligodendrocyte regeneration and remyelination
Astrocytes Are Primed by Chronic Neurodegeneration to Produce Exaggerated Chemokine and Cell Infiltration Responses to Acute Stimulation with the Cytokines IL-1β and TNF-α
Toxicity of cuprizone a Cu(2+) chelating agent on isolated mouse brain mitochondria: a justification for demyelination and subsequent behavioral dysfunction
Nrf2 deficiency increases oligodendrocyte loss, demyelination, neuroinflammation and axonal damage in an MS animal model.
Stereological Investigation of Regional Brain Volumes after Acute and Chronic Cuprizone-Induced Demyelination
Continuous cuprizone intoxication allows active experimental autoimmune encephalomyelitis induction in C57BL/6 mice
High fat diet consumption results in mitochondrial dysfunction, oxidative stress, and oligodendrocyte loss in the central nervous system.
Focal white matter lesions induce long-lasting axonal degeneration, neuroinflammation and behavioral deficits.
Novel Tools and Investigative Approaches for the Study of Oligodendrocyte Precursor Cells (NG2-Glia) in CNS Development and Disease.
Astrocytes & Neurodegeneration
Astrocytes are important for the health and function of the central nervous system. When these cells stop functioning properly, either through gain of function or loss of homeostatic controls, neurodegenerative diseases can occur. Here is the latest research on astrocytes and neurodegeneration.
Astrocytes are glial cells that support the blood-brain barrier, facilitate neurotransmission, provide nutrients to neurons, and help repair damaged nervous tissues. Here is the latest research.
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