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Title[redir]:
Degeneration and impaired regeneration of gray matter oligodendrocytes in amyotrophic lateral sclerosis | Nature Neuroscience
Description:
Oligodendrocytes form myelin sheaths and provide metabolic support to axons. Using in vivo genetic fate tracing in a mouse model of amyotrophic lateral sclerosis (ALS), this study shows that there is extensive degeneration of oligodendrocytes near motor neurons prior to behavioral manifestation of disease. Although oligodendrocytes were regenerated from resident progenitors, they failed to mature and restore myelin, a feature also observed in brain and spinal cord tissue from ALS patients. Selective deletion of ALS-linked mutant SOD1 from the oligodendrocyte lineage greatly delayed disease onset, suggesting that this mutant protein impairs their ability to support motor neurons. Oligodendrocytes associate with axons to establish myelin and provide metabolic support to neurons. In the spinal cord of amyotrophic lateral sclerosis (ALS) mice, oligodendrocytes downregulate transporters that transfer glycolytic substrates to neurons and oligodendrocyte progenitors (NG2+ cells) exhibit enhanced proliferation and differentiation, although the cause of these changes in oligodendroglia is unknown. We found extensive degeneration of gray matter oligodendrocytes in the spinal cord of SOD1 (G93A) ALS mice prior to disease onset. Although new oligodendrocytes were formed, they failed to mature, resulting in progressive demyelination. Oligodendrocyte dysfunction was also prevalent in human ALS, as gray matter demyelination and reactive changes in NG2+ cells were observed in motor cortex and spinal cord of ALS patients. Selective removal of mutant SOD1 from oligodendroglia substantially delayed disease onset and prolonged survival in ALS mice, suggesting that ALS-linked genes enhance the vulnerability of motor neurons and accelerate disease by directly impairing the function of oligodendrocytes.
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Keywords {๐}
pubmed, article, google, scholar, cas, nature, central, mice, neurosci, sclerosis, oligodendrocytes, human, amyotrophic, lateral, cell, oligodendrocyte, analysis, access, matter, spinal, cord, sod, glial, supplementary, degeneration, neurons, cells, motor, mutant, content, disease, adult, brain, expression, university, school, research, fig, rothstein, nat, axonal, usa, johns, hopkins, institute, medicine, cookies, neuroscience, gray, kang,
Topics {โ๏ธ}
nature portfolio permissions reprints privacy policy advertising disease research center als-linked genes enhance social media als research nature 468 nature 487 nature 485 nature 425 nature cre/lox animal study long-term memory formation sactl-va biorepository trust cytokine-induced cell death amyotrophic lateral sclerosis plp-overexpressing transgenic rats elicit anti-cns immunity neuronalโglial communication perturbations tau-positive glial inclusions providing plp1-creer mice inducible site-specific recombination springerlink instant access personal data content oligodendrocyte failure long-term axonal integrity ng2-expressing cell astrocyte-neuron lactate transport data protection permissions oligodendroglial progenitor cells sod1g93a transgenic rats oligodendrocyte development multiple sclerosis lesions mutant human tau insoluble alpha-synuclein mutant human cu exhibit enhanced proliferation brain development mutant sod1g93a mice primary oligodendrocyte death privacy adult human brain gene expression atlas johns hopkins school cre-mediated excision spinal cord transfer glycolytic substrates
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description:Oligodendrocytes form myelin sheaths and provide metabolic support to axons. Using in vivo genetic fate tracing in a mouse model of amyotrophic lateral sclerosis (ALS), this study shows that there is extensive degeneration of oligodendrocytes near motor neurons prior to behavioral manifestation of disease. Although oligodendrocytes were regenerated from resident progenitors, they failed to mature and restore myelin, a feature also observed in brain and spinal cord tissue from ALS patients. Selective deletion of ALS-linked mutant SOD1 from the oligodendrocyte lineage greatly delayed disease onset, suggesting that this mutant protein impairs their ability to support motor neurons. Oligodendrocytes associate with axons to establish myelin and provide metabolic support to neurons. In the spinal cord of amyotrophic lateral sclerosis (ALS) mice, oligodendrocytes downregulate transporters that transfer glycolytic substrates to neurons and oligodendrocyte progenitors (NG2+ cells) exhibit enhanced proliferation and differentiation, although the cause of these changes in oligodendroglia is unknown. We found extensive degeneration of gray matter oligodendrocytes in the spinal cord of SOD1 (G93A) ALS mice prior to disease onset. Although new oligodendrocytes were formed, they failed to mature, resulting in progressive demyelination. Oligodendrocyte dysfunction was also prevalent in human ALS, as gray matter demyelination and reactive changes in NG2+ cells were observed in motor cortex and spinal cord of ALS patients. Selective removal of mutant SOD1 from oligodendroglia substantially delayed disease onset and prolonged survival in ALS mice, suggesting that ALS-linked genes enhance the vulnerability of motor neurons and accelerate disease by directly impairing the function of oligodendrocytes.
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