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Journal ArticleDOI

The role of myelin and oligodendrocytes in axonal energy metabolism.

TLDR
Studying axo-glial signalling and energy metabolism will lead to a better understanding of neurodegenerative diseases, in which axonal energy metabolism fails, including neurological disorders as diverse as multiple sclerosis, leukodystrophies, and amyotrophic lateral sclerosis.
About
This article is published in Current Opinion in Neurobiology.The article was published on 2013-12-01. It has received 260 citations till now. The article focuses on the topics: Myelin.

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Citations
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Journal ArticleDOI

Myelin Protection by Ursolic Acid in Cuprizone-Induced Demyelination in Mice.

TL;DR: The finding indicated that UA could decrease the extent of demyelination area and enhanced myelin stain intensity within CC and protected oligodendrocyte lineage cells against cuprizone toxin indicated that myelinated structures could be protected by UA in corpus callosum.
Book ChapterDOI

Effects on Glial Cell Glycolysis in Schizophrenia: An Advanced Aging Phenotype?

TL;DR: Given the role of glial cells in brain energy metabolism, the association of glycolysis dysfunction and the accelerated aging of neuronal cells in schizophrenia, studies focusing on those aspects can yield important insights into the causes and implications of the disorder.
Journal ArticleDOI

White-Matter Repair as a Novel Therapeutic Target for Early Adversity

TL;DR: Early adversity (EA) impairs myelin development in a manner that persists later in life across diverse mammalian species including humans, non-human primates, and rodents as discussed by the authors, and this area of translational research has received relatively little attention and no comprehensive review is currently available to address these issues.
Journal ArticleDOI

Myelination May Be Impaired in Neonates Following Birth Asphyxia

TL;DR: A T2* mapping sequence was used to assess myelination in healthy and critically ill neonates with neonatal encephalopathy and found that birth asphyxia, in addition to causing the previously well-described direct injury to the brain, may impair myelinations.
References
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Journal ArticleDOI

Axonal transection in the lesions of multiple sclerosis.

TL;DR: Transected axons are common in the lesions of multiple sclerosis, and axonal transection may be the pathologic correlate of the irreversible neurologic impairment in this disease.
Journal ArticleDOI

Glutamate uptake into astrocytes stimulates aerobic glycolysis: a mechanism coupling neuronal activity to glucose utilization

TL;DR: It is reported that glutamate, in addition to its receptor-mediated actions on neuronal excitability, stimulates glycolysis--i.e., glucose utilization and lactate production--in astrocytes and is consistent with data obtained from functional brain imaging studies indicating local nonoxidative glucose utilization during physiological activation.
Journal ArticleDOI

Multiple Sclerosis: An Immune or Neurodegenerative Disorder?

TL;DR: Data that support neurodegeneration as the major cause of irreversible neurological disability in MS patients are reviewed and it is questioned whether inflammatory demyelination is primary or secondary in the disease process.
Journal ArticleDOI

Axonal damage in acute multiple sclerosis lesions.

TL;DR: The results show the expression of amyloid precursor protein in damaged axons within acute multiple sclerosis lesions, and in the active borders of less acute lesions, which may have implications for the design and timing of therapeutic intervention.
Journal ArticleDOI

Oligodendroglia metabolically support axons and contribute to neurodegeneration

TL;DR: It is shown that the most abundant lactate transporter in the central nervous system, monocarboxylate transporter 1 (MCT1, also known as SLC16A1), is highly enriched within oligodendroglia and that disruption of this transporter produces axon damage and neuron loss in animal and cell culture models.
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