Dietary cholesterol promotes repair of demyelinated lesions in the adult brain

Stefan A. Berghoff, Nina Gerndt, Jan Winchenbach, Sina K. Stumpf, Leon Hosang, Francesca Odoardi, Torben Ruhwedel, Carolin Böhler, Benoit Barrette, Ruth Stassart, David Liebetanz, Payam Dibaj, Wiebke Möbius, Julia M. Edgar and Gesine Saher ()
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Stefan A. Berghoff: Max Planck Institute of Experimental Medicine
Nina Gerndt: Max Planck Institute of Experimental Medicine
Jan Winchenbach: Max Planck Institute of Experimental Medicine
Sina K. Stumpf: Max Planck Institute of Experimental Medicine
Leon Hosang: Institute of Neuroimmunology and Institute for Multiple Sclerosis Research, University Medical Centre Göttingen
Francesca Odoardi: Institute of Neuroimmunology and Institute for Multiple Sclerosis Research, University Medical Centre Göttingen
Torben Ruhwedel: Max Planck Institute of Experimental Medicine
Carolin Böhler: Max Planck Institute of Experimental Medicine
Benoit Barrette: Max Planck Institute of Experimental Medicine
Ruth Stassart: Max Planck Institute of Experimental Medicine
David Liebetanz: Georg-August University
Payam Dibaj: Max Planck Institute of Experimental Medicine
Wiebke Möbius: Max Planck Institute of Experimental Medicine
Julia M. Edgar: Max Planck Institute of Experimental Medicine
Gesine Saher: Max Planck Institute of Experimental Medicine

Nature Communications, 2017, vol. 8, issue 1, 1-15

Abstract: Abstract Multiple Sclerosis (MS) is an inflammatory demyelinating disorder in which remyelination failure contributes to persistent disability. Cholesterol is rate-limiting for myelin biogenesis in the developing CNS; however, whether cholesterol insufficiency contributes to remyelination failure in MS, is unclear. Here, we show the relationship between cholesterol, myelination and neurological parameters in mouse models of demyelination and remyelination. In the cuprizone model, acute disease reduces serum cholesterol levels that can be restored by dietary cholesterol. Concomitant with blood-brain barrier impairment, supplemented cholesterol directly supports oligodendrocyte precursor proliferation and differentiation, and restores the balance of growth factors, creating a permissive environment for repair. This leads to attenuated axon damage, enhanced remyelination and improved motor learning. Remarkably, in experimental autoimmune encephalomyelitis, cholesterol supplementation does not exacerbate disease expression. These findings emphasize the safety of dietary cholesterol in inflammatory diseases and point to a previously unrecognized role of cholesterol in promoting repair after demyelinating episodes.

Date: 2017
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DOI: 10.1038/ncomms14241

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