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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

Neuron–oligodendrocyte interaction in neuroinflammation

TL;DR: The present review summarizes the current basic knowledge of the mutual relationship between axons and oligodendrocytes with relevance to MS research and realizes that the oligodends is not just a partner for saltatory conduction.
Journal ArticleDOI

Superfood for axons: Glial exosomes boost axonal energetics by delivery of SIRT2.

TL;DR: Chamberlain et al. as mentioned in this paper provided evidence that oligodendrocyte-to-axon transfer of SIRT2 via extracellular vesicles (exosomes) enables deacetylation of mitochondrial proteins, enhancing axonal energy production.
Journal ArticleDOI

Association of aerobic glycolysis with the structural connectome reveals a benefit-risk balancing mechanism in the human brain.

TL;DR: In this paper, a weighted regional distance-dependent model was proposed to estimate the total axonal projection length of a brain node, with higher levels located in the default-mode and prefrontal regions.
Journal ArticleDOI

Dysfunction of oligodendrocyte inwardly rectifying potassium channel in a rat model of amyotrophic lateral sclerosis.

TL;DR: In this article, the authors examined the functional properties of oligodendrocytes in the SOD1G93A rat model of ALS with a particular focus on the inwardly rectifying potassium channel Kir4.1.
Book ChapterDOI

Visualization and Time-Lapse Microscopy of Myelinating Glia In Vivo in Zebrafish.

TL;DR: The generation and use of transgenic zebrafish are described and use is described to visualize dynamics of myelinating glia using cell type-specific expression and microscopy of genetically encoded fluorescent proteins.
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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