Oligodendroglia metabolically support axons and contribute to neurodegeneration

Youngjin Lee, Brett M. Morrison, Yun Li, Sylvain Lengacher, Mohamed H. Farah, Paul N. Hoffman, Yiting Liu, Akivaga Tsingalia, Lin Jin, Ping-Wu Zhang, Luc Pellerin, Pierre J. Magistretti and Jeffrey D. Rothstein ()
Additional contact information
Youngjin Lee: The Johns Hopkins University, 855 North Wolfe Street, Rangos 248, Baltimore, Maryland 21205, USA
Brett M. Morrison: The Johns Hopkins University, 855 North Wolfe Street, Rangos 248, Baltimore, Maryland 21205, USA
Yun Li: The Johns Hopkins University, 855 North Wolfe Street, Rangos 248, Baltimore, Maryland 21205, USA
Sylvain Lengacher: School of Life Sciences, Brain Mind Institute, Ecole Polytechnique Federale de Lausanne (EPFL), Station 19, CH-1015 Lausanne, Switzerland
Mohamed H. Farah: The Johns Hopkins University, 855 North Wolfe Street, Rangos 248, Baltimore, Maryland 21205, USA
Paul N. Hoffman: The Johns Hopkins University, 855 North Wolfe Street, Rangos 248, Baltimore, Maryland 21205, USA
Yiting Liu: The Johns Hopkins University, 855 North Wolfe Street, Rangos 248, Baltimore, Maryland 21205, USA
Akivaga Tsingalia: The Johns Hopkins University, 855 North Wolfe Street, Rangos 248, Baltimore, Maryland 21205, USA
Lin Jin: The Johns Hopkins University, 855 North Wolfe Street, Rangos 248, Baltimore, Maryland 21205, USA
Ping-Wu Zhang: The Johns Hopkins University, 855 North Wolfe Street, Rangos 248, Baltimore, Maryland 21205, USA
Luc Pellerin: University of Lausanne, 7 Rue du Bugnon, CH-1005 Lausanne, Switzerland
Pierre J. Magistretti: School of Life Sciences, Brain Mind Institute, Ecole Polytechnique Federale de Lausanne (EPFL), Station 19, CH-1015 Lausanne, Switzerland
Jeffrey D. Rothstein: The Johns Hopkins University, 855 North Wolfe Street, Rangos 248, Baltimore, Maryland 21205, USA

Nature, 2012, vol. 487, issue 7408, 443-448

Abstract: Abstract Oligodendroglia support axon survival and function through mechanisms independent of myelination, and their dysfunction leads to axon degeneration in several diseases. The cause of this degeneration has not been determined, but lack of energy metabolites such as glucose or lactate has been proposed. Lactate is transported exclusively by monocarboxylate transporters, and changes to these transporters alter lactate production and use. Here we show 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. In addition, this same transporter is reduced in patients with, and in mouse models of, amyotrophic lateral sclerosis, suggesting a role for oligodendroglial MCT1 in pathogenesis. The role of oligodendroglia in axon function and neuron survival has been elusive; this study defines a new fundamental mechanism by which oligodendroglia support neurons and axons.

Date: 2012
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DOI: 10.1038/nature11314

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