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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.
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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

A Cellular Perspective on Brain Energy Metabolism and Functional Imaging

TL;DR: This article aims at providing an integration of brain energy metabolism across resolution scales with decisive insights into the understanding of the cellular and molecular bases of the coupling between neuronal activity and energy metabolism.
Journal ArticleDOI

Lactate in the brain: from metabolic end-product to signalling molecule

TL;DR: Overall, lactate ensures adequate energy supply, modulates neuronal excitability levels and regulates adaptive functions in order to set the 'homeostatic tone' of the nervous system.
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Axonal transport: cargo-specific mechanisms of motility and regulation

TL;DR: An overview of axonal transport pathways is provided and their role in neuronal function is discussed and Retrograde transport, which plays a major role in neurotrophic and injury response signaling, is discussed.
Journal ArticleDOI

New Horizons in Diabetic Neuropathy: Mechanisms, Bioenergetics, and Pain

TL;DR: The structural components of the peripheral nervous system that underlie its susceptibility to metabolic insults are presented and the pathways that contribute to peripheral nerve injury in DN are discussed.
Journal ArticleDOI

Oligodendrocytes: Myelination and Axonal Support

TL;DR: The current understanding of how myelin is generated and also the role of oligodendrocytes in supporting the long-term integrity of myelinated axons are summarized.
References
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Journal ArticleDOI

Molecular Disruptions of the Panglial Syncytium Block Potassium Siphoning and Axonal Saltatory Conduction: Pertinence to Neuromyelitis Optica and other Demyelinating Diseases of the Central Nervous System

TL;DR: A common thread linking several CNS demyelinating diseases is the disruption of potassium siphoning/water transport within the panglial syncytium, and additional components required by myelinated axons for a newly-described process of voltage-augmented "dynamic" potassium siphoned.
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Mice lacking COX10 in skeletal muscle recapitulate the phenotype of progressive mitochondrial myopathies associated with cytochrome c oxidase deficiency

TL;DR: This mouse model with an isolated cytochrome c oxidase (COX) deficiency by disrupting the COX10 gene in skeletal muscle allowed us to correlate the muscle function with residual COX activity, an estimate that can help predict the progression pattern of human mitochondrial myopathies.
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White matter integrity and vulnerability to Alzheimer's disease: preliminary findings and future directions.

TL;DR: The present review summarizes recent evidence suggesting that WM integrity declines are present in individuals at high AD-risk, prior to cognitive decline, and DTI holds promise as a method to aid identification of presymptomatic AD.
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Genetically Induced Adult Oligodendrocyte Cell Death Is Associated with Poor Myelin Clearance, Reduced Remyelination, and Axonal Damage

TL;DR: This model provides the opportunity to study the consequences of adult oligodendrocyte death in the absence of primary axonal injury and reactive cells of the adaptive immune system, and indicates that if the blood–brain barrier is not disrupted, myelin debris is not removed efficiently, remyelination is impaired, and axonal integrity is compromised, likely as the result of myelin detachment.
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Primary oligodendrocyte death does not elicit anti-CNS immunity

TL;DR: This paper showed that diffuse oligodendrocyte death alone or in conjunction with immune activation does not trigger anti-CNS immunity, and this lack of reactivity was not mediated by enhanced myelin-specific tolerance.
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