CPT1A and amyotrophic lateral sclerosis: Pathological states involving lipid overload, illustrated by models of amyotrophic lateral sclerosis, exhibit increased PLIN2 expression along with the downregulation of the lipolytic enzyme ATGL and the mitochondrial fatty acid oxidation enzyme carnitine palmitoyltransferase 1A (CPT1A), resulting in disrupted lipid metabolism, mitochondrial dysfunction, and intramyocellular lipotoxicity (30).