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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

Glia in mammalian development and disease.

TL;DR: The origins of glia are reviewed, their diverse roles during neural development and their contribution to plasticity and disease in the adult mammalian nervous system are discussed.
Journal ArticleDOI

Activation of SIRT3 by the NAD+ Precursor Nicotinamide Riboside Protects from Noise-Induced Hearing Loss

TL;DR: It is found that administration of NR, even after noise exposure, prevents noise-induced hearing loss (NIHL) and spiral ganglia neurite degeneration and is mediated by the NAD(+)-dependent mitochondrial sirtuin, SIRT3.
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Compartment-Specific Regulation of Autophagy in Primary Neurons.

TL;DR: It is found that at steady state, the cell soma contains populations of autophagosomes derived from distinct neuronal compartments and defined by differences in maturation state and dynamics, suggesting that constitutive autophagy in neurons maintains homeostasis by playing an integral role in regulating the quality of the neuronal proteome.
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Accelerated remyelination during inflammatory demyelination prevents axonal loss and improves functional recovery

TL;DR: Oligodendroglial-specific genetic ablation of the M1 muscarinic receptor, a potent negative regulator of oligodendrocyte differentiation and myelination results in accelerated remyelination, preventing axonal loss and improving functional recovery, and demonstrates that accelerated remYelination supports axonal integrity and neuronal function after inflammatory demyelinated.
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Myelin damage and repair in pathologic CNS: challenges and prospects.

TL;DR: The precise organization of myelinated axons and the reciprocal axo-myelin interactions that warrant properly balanced physiological activities within the CNS are provided and the current status of cell-based therapies for promoting remyelination is provided.
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.
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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.
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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.
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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.
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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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