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This article is more than five years old. Autism research - and science in general - is constantly evolving, so older articles may contain information or theories that have been reevaluated since their original publication date.
‘Sleeping like a baby’ is more than just a figure of speech. It’s actually a fair description of what happens when we close our eyes at night, and even during daytime naps. The brain returns to a kind of developmental state, shaping and pruning neural circuits to enhance learning and memory.
It’s been unclear whether this is a cause or an effect of the diminished synaptic plasticity associated with autism. Synaptic plasticity is the ability of synapses, the junctions between neurons, to modulate their strength in response to the use or disuse of a particular pathway. This process underlies learning and memory and is known to be disrupted in Rett and fragile X syndromes, and in autism.
In a new review published in the September issue of Trends in Neurosciences, researchers at the Stanford Center for Sleep Sciences and Medicine in Palo Alto, California suggest that sleep problems in neurodevelopmental disorders don’t just reflect an underlying weakness in synaptic plasticity. They may actively intensify the aberrant synaptic plasticity in these disorders.
A study earlier this year reported that children with autism spend less time in the rapid eye movement (REM) phase of sleep than do either typically developing children or those with developmental delays. But studies show that they are also deprived of non-REM sleep and slow-wave sleep, in which undulating waves of electrical activity sweep through the cortex.
In the first phase of slow-wave sleep, which commences in the first 15 minutes after mammals fall asleep, memory traces stored in circuits in the hippocampus and cortex are replayed. Researchers believe that this is when some synaptic pathways are consolidated while others are pruned. Insomnia and restless sleep subverts this process.
Researchers have teased out some of the mechanisms associated with disrupted sleep in autism-associated syndromes. Loss of the fragile X syndrome protein FMRP, for example, turns fruit flies into restless sleepers. Mice lacking the protein also sleep for shorter periods of time, much as do individuals with autism.
This is not surprising, as research has shown that sleep is conserved across species: Even worms sleep. In worms, a sleep-like state called lethargus is induced by a signaling pathway known to be involved in synaptic plasticity in mammals.
Sleep appears to induce a state of structural and molecular super-plasticity, the Stanford researchers say, focused not on taking in new information, as during waking hours, but on prioritizing and consolidating known information.
It’s become clear that the heightened synaptic plasticity that occurs during sleep is conserved across circuits, developmental stages and species, according to the review.
Another study published in the August issue of the Journal of Child and Adolescent Psychopharmacology shows that donepezil, a drug used to treat Alzheimer’s-related dementia, increases REM sleep in a small group of children with autism with sleep problems.
Enhancing sleep in children with autism could improve some of the behaviors associated with the disorder. And studying sleep in the context of autism might also help researchers understand why flies and worms, mice and men all benefit from a good snooze.