Ketogenic diet ameliorates axonal defects and promotes myelination in Pelizaeus–Merzbacher disease

Sina K. Stumpf(Max Planck Institute of Experimental Medicine), Stefan A. Berghoff(Max Planck Institute of Experimental Medicine), Andrea Trevisiol(Max Planck Institute of Experimental Medicine), Lena Spieth(Max Planck Institute of Experimental Medicine), Tim Düking(Max Planck Institute of Experimental Medicine), Lennart V. Schneider(Max Planck Institute of Experimental Medicine), Lennart Schlaphoff(Max Planck Institute of Experimental Medicine), Steffi Dreha‐Kulaczewski(University of Göttingen), Annette Bley(Universität Hamburg), Dinah Burfeind(Max Planck Institute of Experimental Medicine), Kathrin Kusch(Max Planck Institute of Experimental Medicine), Mišo Mitkovski(Max Planck Institute of Experimental Medicine), Torben Ruhwedel(Max Planck Institute of Experimental Medicine), Philipp Guder(Universität Hamburg), Heiko Röhse(Max Planck Institute of Experimental Medicine), Jonas Denecke(Universität Hamburg), Jutta Gärtner(University of Göttingen), Wiebke Möbius(Nanoscale Microscopy and Molecular Physiology of the Brain Cluster of Excellence 171 — DFG Research Center 103), Klaus‐Armin Nave(Nanoscale Microscopy and Molecular Physiology of the Brain Cluster of Excellence 171 — DFG Research Center 103), Gesine Saher(Max Planck Institute of Experimental Medicine)
Acta Neuropathologica
March 27, 2019
Cited by 79Open Access
Full Text

Abstract

Pelizaeus-Merzbacher disease (PMD) is an untreatable and fatal leukodystrophy. In a model of PMD with perturbed blood-brain barrier integrity, cholesterol supplementation promotes myelin membrane growth. Here, we show that in contrast to the mouse model, dietary cholesterol in two PMD patients did not lead to a major advancement of hypomyelination, potentially because the intact blood-brain barrier precludes its entry into the CNS. We therefore turned to a PMD mouse model with preserved blood-brain barrier integrity and show that a high-fat/low-carbohydrate ketogenic diet restored oligodendrocyte integrity and increased CNS myelination. This dietary intervention also ameliorated axonal degeneration and normalized motor functions. Moreover, in a paradigm of adult remyelination, ketogenic diet facilitated repair and attenuated axon damage. We suggest that a therapy with lipids such as ketone bodies, that readily enter the brain, can circumvent the requirement of a disrupted blood-brain barrier in the treatment of myelin disease.


Related Papers