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ABSENCE OF COMPACT CORTICAL MYELIN RESULTS IN REMARKABLY NORMAL HIGHER BRAIN FUNCTIONS
Anne-Fleur Wildenburgand 18 co-authors
Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS02-07PM-465
Presentation
Date TBA
Board: PS02-07PM-465
Event Information
Poster Board
PS02-07PM-465
Poster
View posterAbstract
While myelin and oligodendrocytes have been studied for decades, their role on higher brain function and cognition remain to be elucidated. CNS myelin is not restricted to white matter tracts, but is also abundant in the forebrain. Moreover patients with leukodystrophies exhibit both motor and sensory defects as well as cognitive impairment, suggesting a role in higher brain functions. However, in leukodystrophy patients the impact of myelin deficiency cannot be distinguished from the secondary (dysmyelination-induced) loss of axonal integrity. To specifically investigate the role of cortical myelin without interference by basic brain and motor dysfunctions, we generated a novel mouse mutant, in which a floxed Myelin basic protein (Mbp) allele is deleted in Emx1-Cre expressing ventricular zone stem cells of the forebrain. The resulting MBPcKO mice are fully myelinated, except for a severe dysmyelination of the dorsal telencephalon, including isocortex, corpus callosum, and hippocampus. Histological analysis of MBPcKO confirmed the near-complete absence of MBP in the recombined forebrain. Surprisingly, comprehensive behavioral testing from 2 to 24 months revealed no gross abnormalities in motor function, learning and memory, anxiety, or executive functions. Using multi-unit recordings in the auditory and prefrontal cortex, we determined some neuronal fatigue, suggesting deficits in axonal energy metabolism in the myelin-deficient cortex. These findings support a working model, in which cortical myelination in mice is more likely to preserve rather than optimize axon function and synaptic circuitries.
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