Abstract
Axons in the adult mammalian nervous system can extend over formidable distances, up to one meter or more in humans. During development, axonal and dendritic growth requires continuous addition of new membrane. Of the three major kinds of membrane lipids, phospholipids are the most abundant in all cell membranes, including neurons. Not only immature axons, but also severed axons in the adult require large amounts of lipids for axon regeneration to occur. Lipids also serve as energy storage, signaling molecules and they contribute to tissue physiology, as demonstrated by a variety of metabolic disorders in which harmful amounts of lipids accumulate in various tissues through the body. Detrimental changes in lipid metabolism and excess accumulation of lipids contribute to a lack of axon regeneration, poor neurological outcome and complications after a variety of central nervous system (CNS) trauma including brain and spinal cord injury. Recent evidence indicates that rewiring lipid metabolism can be manipulated for therapeutic gain, as it favors conditions for axon regeneration and CNS repair. Here, we review the role of lipids, lipid metabolism and ectopic lipid accumulation in axon growth, regeneration and CNS repair. In addition, we outline molecular and pharmacological strategies to fine-tune lipid composition and energy metabolism in neurons and non-neuronal cells that can be exploited to improve neurological recovery after CNS trauma and disease.
Highlights
Developing axons in the mammalian nervous system can extend very long distances [1]
Membrane proteins tend to accumulate within specialized microdomains the plasma membrane called lipid rafts that are rich in cholesterol and sphingolipi Whereas axons in the mammalian peripheral nervous system spontaneously regener over long distances
We have discussed evidence suggesting that reprogramming lipid metabolism, boosting mitochondrial transport and neuron-glia metabolic coupling promote survival and regeneration of injured axons
Summary
Developing axons in the mammalian nervous system can extend very long distances [1]. After reaching their targets, axons integrated into functional circuits continue to extend via mechanisms of stretch growth as the body continues to grow [2,3]. Membrane proteins tend to accumulate within specialized microdomains the plasma membrane called lipid rafts that are rich in cholesterol and sphingolipi Whereas axons in the mammalian peripheral nervous system spontaneously regener over long distances [9,10], theincentral nervous system (CNS)Whereas fail to mount a su membrane called lipid rafts axons that areinrich cholesterol and sphingolipids. Regeneration failure causes long term stru distances [9,10], axons in the central nervous system (CNS)trauma fail to mount a successful tural and functional impairment after a variety of CNS including brain and spin regenerative response [11,12,13]. Lipids are implicated myelin formation and ser axon growth anddiseases regeneration failure after CNS trauma [6,18], but in neurodegenerative. Membrane lipids. (B) Illustration of the typical lipid bilayer of the plasma membrane
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