Lipids are a fundamental class of organic molecules implicated in a wide range 
of biological processes related to their structural diversity, and based on this 
can be broadly classified into five categories; fatty acids, triacylglycerols 
(TAGs), phospholipids, sterol lipids and sphingolipids. Different lipid classes 
play major roles in neuronal cell populations; they can be used as energy 
substrates, act as building blocks for cellular structural machinery, serve as 
bioactive molecules, or a combination of each. In amyotrophic lateral sclerosis 
(ALS), dysfunctions in lipid metabolism and function have been identified as 
potential drivers of pathogenesis. In particular, aberrant lipid metabolism is 
proposed to underlie denervation of neuromuscular junctions, mitochondrial 
dysfunction, excitotoxicity, impaired neuronal transport, cytoskeletal defects, 
inflammation and reduced neurotransmitter release. Here we review current 
knowledge of the roles of lipid metabolism and function in the CNS and discuss 
how modulating these pathways may offer novel therapeutic options for treating 
ALS.