> The presence of a lipid peroxidation sensor at the core of homeostatic sleep control suggests that sleep protects neuronal membranes against oxidative damage. Indeed, brain phospholipids are depleted of vulnerable polyunsaturated fatty acyl chains after enforced waking, and slowing the removal of their carbonylic breakdown products increases the demand for sleep.
(From Discussion)
> Our experiments also suggest, but do not prove beyond doubt, that sleep loss causes widespread lipid peroxidation in the brain. Definitive proof would require a demonstration that peroxidation products accumulate, rather than that polyunsaturated phospholipids are depleted, as we have shown.
hightlights:
(From Abstract)
> The presence of a lipid peroxidation sensor at the core of homeostatic sleep control suggests that sleep protects neuronal membranes against oxidative damage. Indeed, brain phospholipids are depleted of vulnerable polyunsaturated fatty acyl chains after enforced waking, and slowing the removal of their carbonylic breakdown products increases the demand for sleep.
(From Discussion)
> Our experiments also suggest, but do not prove beyond doubt, that sleep loss causes widespread lipid peroxidation in the brain. Definitive proof would require a demonstration that peroxidation products accumulate, rather than that polyunsaturated phospholipids are depleted, as we have shown.