Researchers have demonstrated that lack of sleep in early life can significantly affect critical aspects of brain development, potentially increasing the likelihood of developing autism spectrum disorder.
It’s well established that sleep deprivation in adults can lead to a range of long-term health problems, including a weakened immune system, weight gain, depression, and a heightened risk of dementia.
But what makes sleep deprivation so detrimental?
Sleep is essential from the moment we are born. In infancy, our brains are in the process of forming synapses, the endings of neurons crucial for learning, attention, working memory, and long-term memory. Sleep facilitates the development and interaction of these neurons, laying the foundation for brain function throughout life.
Disruptions to this delicate process—whether from frequent awakenings or separation anxiety—can lead to enduring effects on brain functionality and behavior.
Recently, a study headed by Sean Gay, a graduate student under Graham Diering, PhD, assistant professor at the Department of Cell Biology and Physiology at the UNC School of Medicine, has shed light on how sleep loss during early life impacts critical brain development stages and raises the risk for autism spectrum disorder (ASD). These findings were published in the Proceedings of the National Academy of Sciences.
“The specific consequences of sleep deprivation during development have not been extensively studied,” stated Diering. “Our research indicates that infants and children are particularly susceptible to the harmful effects of sleep disruption. Additionally, we discovered that sleep loss during this vital developmental stage can interact negatively with genetic predispositions for autism spectrum disorder.”
Sleep Disruption and Autism
Sleep problems can be a significant early marker of brain development issues, as well as other neurodevelopmental disorders, including ASD, attention-deficit hyperactivity disorder, and intellectual impairment. More than 80% of individuals with ASD experience sleep disruptions, yet whether these issues are a cause or a consequence of ASD remains unclear.
Diering has focused on how sleep enhances synaptic connections over time—a process known as synaptic plasticity—and how sleep deprivation can lead to cognitive and neurodegenerative disorders. If researchers could elucidate the relationship between sleep patterns and ASD, it could enhance early diagnosis and foster new treatment strategies.
In 2022, the Diering lab aimed to understand how early life sleep disruption might interact with genetic risk factors for ASD, leading to enduring behavioral changes in adulthood. Using mouse models, the researchers found that sleep disruption in the third week of life (comparable to ages 1-2 in humans) resulted in long-lasting deficits in social behavior among male mice genetically predisposed to develop ASD.
A Study on Sleep Compensation
To delve deeper into their findings, the Diering lab investigated how developing and adult mouse models adapt to sleep loss. By employing specialized mouse housing equipped with sensitive sensors, researchers could meticulously monitor the mice’s movements and breathing, allowing accurate tracking of their sleep and wake states.
The research demonstrated that when adult mice experienced significant sleep loss, they compensated by increasing their sleep during their regular active phases. This phenomenon, known as “sleep rebound,” enabled the adults to recover from lost sleep.
However, the younger mice showed no signs of sleep rebound, confirming the researchers’ theory that they may be more vulnerable to the adverse effects of sleep deprivation. The study also indicated that young mice subjected to sleep deprivation performed poorly in learning and memory tasks, whereas the adults exhibited greater resilience post-sleep loss.
The lab then turned its focus to analyzing the effects of sleep and sleep deprivation on synapses, which are vital for neuron communication and play a key role in memory formation and storage. Furthermore, synapses are well-documented for their crucial role in promoting sleep health.
Through various molecular analyses, researchers examined how sleep deprivation impacts synapses. Utilizing advanced protein analysis, they mapped the protein composition and biochemical alterations affecting synapses. The results indicated that sleep deprivation significantly impacted synapse formation in young mice, but not in adults—highlighting a crucial aspect of brain development.
“Our findings provide one of the most extensive datasets on the molecular effects of sleep loss throughout the lifespan,” remarked Diering.
Future Treatment Possibilities for Autism
A key objective of the lab, informed by the molecular insights gained from this study, is to develop the next generation of sleep-based medications for children. Rather than functioning as sedatives, these drugs aim to target synapses to restore normal sleep functions instead of just modifying sleep behavior.
“Development is not something that can be repeated,” emphasized Diering. “Sleep is essential for our entire lives, especially during developmental stages. Gaining a deeper understanding of what we’ve learned will highlight the importance of addressing sleep issues in ASD, potentially leading to novel therapeutic strategies for treating ASD and other developmental disorders.”
