Scientists highlight the negative effects of sleep disruption on early brain development
Sleep deprivation in adults has long been shown to cause lasting mental and physical health issues, such as weakened immunity, weight gain, depression, and an increased risk of dementia. But why does lack of sleep have such immediate consequences?
Sleep plays a crucial role from the moment we are born. As infants, our brains continue forming the ends of neurons, known as “synapses,” which are essential for learning, attention, working memory, and long-term memory. Sleep allows these neurons to grow and connect, establishing brain functions for the rest of life. If this delicate yet vital process is disrupted, either by prolonged wakefulness or separation anxiety, it could lead to permanent brain and behavioral effects.
A new study, led by Sean Gay, a graduate student in the lab of Graham Diering, Ph.D., at the University of North Carolina (UNC) School of Medicine, offers new insights into how sleep loss during early life impacts fundamental parts of brain development and may also increase the risk of autism spectrum disorder (ASD).
“The unique impacts of sleep loss during development are largely unexplored,” said Diering. “Our data show that infants and children are more vulnerable to the negative effects of sleep disruption. We also found that sleep loss during this critical period can interact adversely with the underlying genetic risk for autism spectrum disorder.”
Sleep Disruption and Autism
Sleep problems are a major early indicator of brain developmental issues and other neurodevelopmental disorders, such as ASD, ADHD, and intellectual disability. Sleep disruption has been observed in over 80% of people with ASD, yet it is unclear if it is a cause or consequence of ASD.
Diering has long studied how sleep strengthens synapses over time—a process called synaptic plasticity—and how sleep loss might contribute to cognitive and neurodegenerative disorders. If researchers could better understand the relationship between sleep and ASD, it could lead to earlier diagnoses and new treatment strategies.
In 2022, Diering’s lab aimed to understand whether early-life sleep disruption could interact with genetic ASD risk to cause long-term behavioral changes. Using mouse models, the researchers found that sleep disruption in the third week of life (equivalent to ages 1-2 in humans) led to long-lasting deficits in social behavior in male mice genetically predisposed to ASD.
A Study on Sleep Recovery
Diering’s lab then investigated how adult and developing mouse models compensate for sleep loss. Using specialized mouse houses with highly sensitive sensors, they monitored the mice’s movements and breathing, tracking sleep and wake states.
They found that adult mice compensated for significant sleep loss by increasing sleep during normal activity hours—a response called “sleep recovery.” However, young mice lacked this recovery ability entirely, supporting the researchers’ hypothesis that young mice might be more vulnerable to the harmful effects of sleep deprivation. Additionally, sleep deprivation in young mice fully diminished their performance in a learning memory task, while adults were far more resilient.
Next, the lab focused on the effects of sleep and sleep deprivation on neuronal synapses, which facilitate communication between neurons and play a central role in memory formation and storage. The researchers conducted a series of molecular analyses to examine how sleep deprivation affects synapses. Using advanced protein analysis, they mapped protein composition and biochemical changes impacting synapses. They found that sleep deprivation significantly affected synapse formation in young mice, a key aspect of brain development.
“This now provides one of the largest and most comprehensive datasets on the molecular effects of sleep loss across the lifespan,” said Diering.
Future Pathways for Autism Treatments
An ongoing goal of Diering’s lab, guided by this study’s molecular work, is to develop next-generation sleep-based drugs for children. Rather than acting as a sedative, they hope to create a drug that targets synapses to restore sleep function without altering sleep behavior itself.
“Development is not something you can go back and redo,” says Diering. “Sleep is essential throughout life, especially during development. Understanding what we now know will emphasize the importance of addressing sleep issues in ASD and could lead to significant therapeutic approaches for ASD and other developmental conditions.”
