Abstract
The mammalian brain exhibits unique regulation of fatty acid metabolism, yet the capacity and relevance for mitochondrial fatty acid β-oxidation (FAO) in the mammalian nervous system remain unclear. Dysregulated FAO is associated with neurologic disorders, and the elevation of intermediates in FAO is observed in nervous system trauma and neurodegeneration. White et al. (e00037-20) have characterized the biochemical and physiological role of FAO in the nervous system using mice with a conditional, pan-brain-specific loss of FAO. They demonstrate that the brain oxidizes a substantial quantity of long-chain fatty acids independently of diet or metabolic state.
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