I’ve always been fascinated by how our brain works during sleep, especially the Delta state. Pretty sure the most of you too. Imagine slipping into a deep, restful sleep during the earliest and most profound cycles of the night. This is when your brain starts producing slow, high-amplitude waves known as delta waves, oscillating gently at a frequency of about 0.5 to 4 Hz. During this time, brain activity slows down, allowing your body and mind to step back from the day’s stimuli and enter a period of profound rest.
The importance of Delta sleep for our health and well-being is immense. It plays a crucial role in helping our bodies recover physically by releasing growth hormones, strengthening the immune system, and reducing stress. What I find particularly fascinating is that during this deep sleep state, our memories get consolidated, synaptic connections reorganize, and the brain essentially “resets” itself for a new day. Without enough of this deep, slow-wave sleep, both our body and mind can suffer, leading to poor memory, reduced ability to learn, a weakened immune response, and imbalanced stress regulation.
In this essay, I want to guide you through a clear and comprehensive view of the Delta state. We’ll start by defining its main characteristics and seeing how it differs from other sleep phases. Then, we’ll explore its roles in physical and mental health, sharing insights I’ve gathered that I hope will resonate with you. We’ll also look at how researchers measure and investigate deep sleep. Finally, we’ll discuss conditions that can disrupt this state and consider strategies to promote and protect it, offering my perspective on maintaining healthy sleep patterns.
Definition and Characterization of the Delta State
I find the Delta state of the brain truly interesting, and I’m excited to share some insights about this deep sleep phase with you. Picture your brain entering a state of slow-wave sleep, mainly during the early part of the night. This phase is marked by what we call delta waves, which occur when neurons across large areas of the brain start synchronizing. These waves usually oscillate at frequencies from about 0.5 to 4 Hz, showing a significant decrease in neuron activity. What’s remarkable is the amplitude of these waves, often exceeding 75 microvolts and sometimes going well above 100 microvolts, showcasing strong synchronization.
The time spent in the Delta state varies from person to person and night to night but generally occurs during the first two non-REM cycles, making up nearly 20% of total sleep in healthy adults. It usually defines the third stage of non-REM sleep, often referred to as slow-wave sleep (SWS), indicating when the body reaches its most restful state. During this time, heart rate, blood pressure, and metabolic activity decrease, reflecting deep relaxation and a temporary reduction in the body’s energy needs.
This slow-wave activity is quite different from other sleep phases, particularly REM sleep, which is characterized by fast, low-amplitude brain activity, vivid dreams, and increased brain metabolic activity. While the Delta state features reduced neuron communication and strong synchronization across large neuron groups, REM sleep is more desynchronized.
Additionally, the Delta state is less responsive to external stimuli, making it less likely for minor disturbances to wake the sleeper. This deep activity offers the body and mind a chance to repair, regenerate, and reorganize neuron circuits in preparation for waking. The distinct features of this state highlight its unique role in human health.
Functions and Significance of Delta Sleep
Exploring the depths of Delta sleep has revealed to me just how crucial this phase is for our body’s repair and regeneration. It’s during this deeply restful state that our physiological repair mechanisms kick into high gear. In this slow-wave phase, our body’s metabolic demands decrease—our heart rate slows, breathing becomes steady and calm, and muscle activity reaches its lowest point. This deceleration opens a window for essential repair and renewal processes. Damaged tissues and cells get restored, growth hormones are released in larger quantities, and proteins necessary for repair are produced more rapidly. This surge in growth factors helps strengthen and rebuild muscles, bones, and even our nervous system, showcasing the physical benefits of deep sleep.
What truly captures my interest is how Delta sleep extends its influence beyond mere physical recovery; it plays a pivotal role in memory consolidation and strengthening neuronal circuits. During this state, the hippocampus, a vital region for memory formation, effectively communicates with the cerebral cortex to transfer new memories into long-term storage. This process, known as memory consolidation, relies on the slow oscillations that act as a timing signal for neuronal activity. These oscillations allow memories to be replayed and integrated into existing networks. The large, slow waves characteristic of Delta sleep provide a unique opportunity for our nervous system to reorganize its synaptic connections, reinforcing those that hold valuable knowledge and weakening those less used. Consequently, deep sleep directly enhances our learning capabilities, problem-solving skills, and creativity upon waking.
The impact of Delta sleep also extends to our immune system and overall health. During this phase, the production and release of cytokines—key players in our immune response—are boosted, enhancing our ability to fight off infections. Additionally, the reduced stress physiology during deep sleep, with lower levels of adrenaline and norepinephrine and decreased activity in the HPA axis, helps conserve energy for protective mechanisms. Components of the adaptive immune response, such as T-cell proliferation and the release of protective cytokines, are particularly active during this period, underscoring the link between deep sleep and a robust immune system.
The benefits of slow-wave sleep touch on various aspects of our physiology, from metabolic regulation and glucose balance to cardiovascular health and resistance to neurodegenerative diseases. There’s increasing evidence that deep sleep aids in clearing metabolic waste from the brain through the glymphatic system, thereby reducing the buildup of neurotoxic proteins like beta-amyloid and tau, which are linked to conditions such as Alzheimer’s disease. Proper slow-wave activity also supports balanced neuroendocrine signals, aiding in the regulation of stress responses and the release of key hormones.
Collectively, these mechanisms highlight the central role of Delta sleep in maintaining our health and functionality. Without sufficient slow-wave sleep, our body’s ability to repair itself, consolidate memories, regulate stress, and defend against disease is significantly impaired. Thus, understanding and safeguarding this stage of sleep is not just about rest—it’s fundamental for physical renewal, cognitive function, and overall well-being.
Measurement of Delta Activity
Understanding how Delta sleep is measured has been quite an eye-opener. In humans, slow-wave or Delta sleep is typically assessed using polysomnography (PSG), the clinical gold standard. This method involves recording scalp electroencephalography (EEG) alongside eye movements and muscle tone. On a scalp EEG, delta waves show up as high-amplitude, slow oscillations, generally around 0.5 to 4 Hz, arising from synchronous cortical firing.
By convention, deep non-REM sleep, also known as Stage N3 or slow-wave sleep, is identified when over 20% of a 30-second period contains these large amplitude delta-frequency waves. According to the AASM manual, N3 or slow-wave sleep is defined as periods where at least 20% of the time shows slow oscillations, roughly 0.5 to 2 Hz, exceeding about 75 μV in peak-to-peak amplitude. In practice, PSG EEG data is filtered to isolate these low frequencies, and technicians identify delta waves by both their frequency and voltage. Automated algorithms also help by quantifying slow-wave activity (SWA) through computing spectral power in the delta band across EEG channels. Essentially, combining multi-channel EEG recording with standard scoring rules allows for reliable detection and quantification of delta oscillations during human sleep.
Landmark Human Studies
Some key human experiments have truly shed light on the functions of Delta sleep. One study that stands out is by Marshall and colleagues in 2006. They applied oscillating transcranial currents at 0.75 Hz to enhance slow oscillations during early non-REM sleep. The results were striking: these induced slow waves significantly increased Stage N3 sleep and improved next-day declarative memory retention compared to a control stimulation. This supports the idea that slow oscillations play a causal role in human memory consolidation, showing that boosting cortical delta activity during sleep leads to better hippocampus-dependent memory.
Complementing this, intracranial recordings in epilepsy patients have shown that during slow-wave sleep, low-frequency signals propagate from the hippocampus to the neocortex, which is the reverse of what we see when we’re awake. This bidirectional “cortical-hippocampal dialogue” model, proposed by Mitra and colleagues in 2016, provides direct evidence in humans that hippocampal memory traces are replayed through delta-band communication during slow-wave sleep.
The importance of Delta sleep in cognition is further highlighted by studies on aging. In a group of healthy adults, Mander and colleagues found that age-related atrophy in the medial prefrontal cortex was associated with reduced non-REM slow-wave activity and impaired overnight memory retention. In other words, older individuals with diminished frontal slow waves showed worse consolidation of episodic memories, suggesting that the deterioration of Delta sleep may contribute to cognitive decline with age.
Similarly, sleep studies in individuals with Alzheimer’s disease have observed that these patients spend less time in Stage N3 and exhibit lower slow-wave activity overall. This reduction in slow-wave sleep correlates with their memory impairments. Specifically, Lee and colleagues noted that individuals with Alzheimer’s showed diminished non-REM slow-wave activity and argued that these slow-wave deficits might both reflect and exacerbate amyloid pathology and learning failures.
Together, these human studies—spanning interventional, imaging, and clinical groups—link delta oscillations to memory processes and brain health, making them cornerstones of our understanding of slow-wave sleep.
Recent Findings and Open Questions
Recent studies have looked into ways to enhance delta sleep, which could benefit memory and brain health, especially as we age or face illnesses. One approach that has gained attention is using noninvasive methods like auditory or electrical stimulation synchronized with the brain’s slow oscillations to strengthen slow-wave activity. In a recent experiment, Wunderlin and colleagues (2023) used multi-night phase-locked acoustic stimulation (PLAS) during slow-wave sleep in older adults. They found lasting improvements in delta-band power and sleep spindle nesting, which were linked to better memory performance even three months later and positive changes in plasma amyloid-β levels. These results hint that improving delta sleep might offer lasting cognitive benefits and support the brain’s clearance of metabolites, opening up promising possibilities for preventing dementia.
However, many questions about delta sleep still need answers. For example, how exactly do slow waves affect memory? How do delta oscillations interact with other brain rhythms during sleep? What leads to the age-related decline in slow-wave activity, and is it reversible? Clinically, researchers are investigating whether issues with slow-wave sleep contribute to cognitive problems in sleep disorders. For instance, people with narcolepsy show almost no delta sleep, as they quickly enter REM sleep, highlighting the role of hypocretin in maintaining deep sleep. Conditions like obstructive sleep apnea and insomnia also disrupt slow-wave sleep, and ongoing studies are examining their impact on memory and brain health.
In essence, tools like EEG and polysomnography help us detect delta waves in the human brain. Important studies by Marshall et al. (2006), Mitra et al. (2016), and Mander et al. (2013) have connected slow oscillations to memory and aging. Current research is focused on delta sleep as a changeable brain process, with methods like auditory, electrical, and drug-based interventions aimed at enhancing slow-wave activity to improve learning and potentially slow brain diseases. This growing body of research continues to shape our understanding of delta sleep, with important implications for both science and medicine.
Research Methods and Findings
Polysomnography (PSG) is widely recognized as the clinical standard for assessing slow-wave, or delta, sleep in humans. During PSG, scalp electroencephalography (EEG) is recorded alongside electrooculography and electromyography to classify sleep stages according to the American Academy of Sleep Medicine (AASM) criteria. Delta waves appear on EEG as high-amplitude oscillations in the 0.5–4 Hz range, often exceeding 75 µV in peak-to-peak voltage. Non-REM Stage 3, or slow-wave sleep (SWS), is identified when at least 20% of a 30-second epoch contains these slow oscillations. Beyond visual scoring, spectral analysis algorithms help quantify slow-wave activity (SWA) by measuring power in the delta band across multiple channels, providing an objective measure of delta sleep intensity.
In a notable intervention, Marshall and colleagues (2006) applied transcranial alternating current stimulation at 0.75 Hz during early non-REM sleep to enhance natural slow waves. Participants receiving this stimulation showed increased SWS duration and significantly improved retention of declarative memories the following morning compared to controls. This study provided compelling evidence that enhancing cortical slow oscillations directly benefits hippocampus-dependent memory consolidation.
Further insights into delta wave propagation have come from intracranial EEG recordings in epilepsy patients. Mitra and colleagues (2016) observed that during SWS, low-frequency oscillatory activity flows from the hippocampus to the neocortex, reversing the information flow seen during wakefulness. This bidirectional “cortical-hippocampal dialogue” supports the idea that hippocampal memory traces are replayed and integrated into cortical networks under slow-wave regulation.
Age-related changes in SWA have been linked to cognitive decline. In a study of healthy older adults, Mander and colleagues (2013) reported that reduced medial prefrontal cortex volume correlated with declines in non-REM SWA and poorer performance on overnight episodic memory tasks. Participants with the lowest frontal SWA showed the greatest deficits in memory retention, suggesting that loss of delta sleep may contribute to age-related memory impairment.
Alzheimer’s disease further highlights the clinical significance of delta sleep. Lee and colleagues (2020) found that patients with Alzheimer’s dementia spent significantly less time in Stage 3 sleep and exhibited lower SWA than age-matched controls. The reduction in slow-wave power correlated with elevated cerebrospinal fluid amyloid-β levels and the severity of memory impairment. These findings suggest that impaired delta sleep may both reflect and worsen amyloid pathology by disrupting the clearance of neurotoxic proteins.
Recent human trials have explored whether enhancing delta sleep can yield lasting benefits. Wunderlin and colleagues (2023) used multi-night phase-locked acoustic stimulation, delivering brief auditory clicks timed to the up-state of natural slow oscillations in older adults. This approach produced lasting increases in SWA and spindle nesting, accompanied by improved memory performance that persisted at a three-month follow-up. Participants also showed reduced plasma amyloid-β concentrations, hinting at potential long-term neuroprotective effects of noninvasive delta enhancement.
Despite these advances, key questions remain. The precise brain circuits that generate and coordinate delta oscillations in aging brains are not fully understood. The interplay between slow waves and other sleep rhythms, such as sleep spindles and hippocampal ripples, requires further study at the cellular level. Developing pharmacological approaches to boost SWA without disrupting overall sleep structure is in early stages and faces challenges in specificity and safety. Clinically, the extent to which sleep disorders like obstructive sleep apnea and chronic insomnia impair delta activity—and thereby accelerate cognitive decline—demands further investigation.
In summary, human sleep research uses EEG and PSG, combined with spectral analysis, to identify and quantify delta wave activity. Groundbreaking studies by Marshall et al. (2006), Mitra et al. (2016), Mander et al. (2013), Lee et al. (2020), and Wunderlin et al. (2023) have shown the functional importance of deep slow-wave sleep for memory consolidation, healthy aging, and potential dementia prevention. Ongoing research aims to map underlying neural circuits, refine noninvasive enhancement techniques, and translate these findings into interventions for sleep-related cognitive disorders.
Disorders of Delta Sleep and Their Consequences
Insomnia and obstructive sleep apnea are two common sleep disorders that significantly reduce the duration and intensity of delta sleep. In cases of primary insomnia, individuals struggle with initiating or maintaining sleep, leading to fragmented non-REM stages and shorter periods of slow-wave sleep. Continuous micro-arousals disrupt the emergence of high-amplitude delta oscillations, decreasing slow-wave activity by up to 40 percent. Obstructive sleep apnea involves repetitive upper-airway collapse, triggering brief arousals that cut short slow-wave epochs prematurely. Those with moderate to severe sleep apnea may lose more than half of their delta sleep time, despite spending a normal amount of time in bed.
A chronic deficit in delta sleep has significant health and cognitive repercussions. Physiologically, reduced slow-wave activity impairs the secretion of growth hormone, weakens immune function, and elevates inflammatory markers. Metabolic dysregulation often follows, with lower delta sleep correlating with insulin resistance and an increased risk of type 2 diabetes. Cardiovascular risks also rise, as disrupted slow-wave sleep is linked to hypertension and elevated resting heart rate. Cognitively, a lack of delta sleep undermines declarative memory consolidation and executive function. Studies show that suppressing slow waves results in performance deficits on verbal recall tasks equivalent to those seen with total sleep deprivation. Longitudinal research indicates that adults with persistently low slow-wave activity are at higher risk of age-related cognitive decline and dementia.
Various therapies aim to restore delta sleep. Continuous Positive Airway Pressure (CPAP) remains the standard treatment for obstructive sleep apnea. By eliminating apneas, CPAP users can recover up to 80 percent of lost slow-wave sleep within weeks. Cognitive Behavioral Therapy for Insomnia (CBT-I) improves sleep continuity and gradually increases slow-wave activity by restructuring maladaptive beliefs and behaviors related to sleep. Emerging noninvasive brain stimulation techniques show promise: slow oscillatory transcranial direct current stimulation during early non-REM sleep enhances slow-wave activity and improves overnight memory retention. Phase-locked auditory stimulation, delivering brief pink noise clicks in synchrony with endogenous up-states, can boost slow-wave activity and spindle coupling without causing arousals, leading to measurable gains in memory consolidation. Pharmacological approaches, such as low-dose gamma-hydroxybutyrate (GHB), increase slow-wave sleep but come with risk profiles that limit their widespread use.
In summary, insomnia and obstructive sleep apnea severely curtail delta sleep, leading to hormonal, immune, metabolic, cardiovascular, and cognitive impairments. Effective treatments, from CPAP and CBT-I to targeted brain stimulation, can restore slow-wave activity and mitigate downstream health risks, highlighting the central role of delta sleep in overall human function.
Disorders of Delta Sleep and Their Consequences
Insomnia and obstructive sleep apnea are two common sleep disorders that greatly reduce the duration and depth of delta sleep. People with insomnia often struggle to fall or stay asleep, leading to interrupted sleep stages and shorter periods of deep sleep. These frequent disruptions prevent the full development of high-amplitude delta waves, reducing slow-wave activity significantly. Obstructive sleep apnea causes repeated interruptions in breathing, leading to brief awakenings that shorten deep sleep phases. Those with moderate to severe sleep apnea may lose more than half of their delta sleep time, even if they spend a normal amount of time in bed.
A persistent lack of delta sleep has wide-ranging effects on health and cognitive function. Physically, reduced slow-wave activity affects the release of growth hormones, weakens the immune system, and increases inflammation. This can lead to issues with metabolism, including insulin resistance and a higher risk of developing type 2 diabetes. Heart health is also impacted, as disrupted deep sleep is linked to high blood pressure and an elevated resting heart rate. Cognitively, insufficient delta sleep impairs memory consolidation and executive function. Research shows that reducing slow waves results in memory performance deficits similar to those seen with complete sleep deprivation. Long-term studies indicate that individuals with consistently low slow-wave activity face a higher risk of cognitive decline and dementia as they age.
Various treatments aim to restore delta sleep. Continuous Positive Airway Pressure (CPAP) is the standard treatment for obstructive sleep apnea. By preventing breathing interruptions, CPAP users can regain up to 80 percent of their lost deep sleep within weeks. Cognitive Behavioral Therapy for Insomnia (CBT-I) improves sleep continuity and gradually increases slow-wave activity by addressing unhelpful beliefs and behaviors related to sleep. New noninvasive brain stimulation techniques show potential: using slow oscillatory transcranial direct current stimulation during early deep sleep enhances slow-wave activity and improves memory retention. Synchronized auditory stimulation, which delivers brief sounds in sync with the brain’s natural rhythms, can enhance slow-wave activity and improve memory consolidation without causing awakenings. While certain medications can increase deep sleep, their side effects limit their widespread use.
To wrap up, insomnia and obstructive sleep apnea significantly reduce delta sleep, leading to hormonal, immune, metabolic, cardiovascular, and cognitive issues. Effective treatments, from CPAP and CBT-I to brain stimulation, can help restore slow-wave activity and reduce associated health risks, emphasizing the importance of delta sleep for overall well-being.
Final Thoughts
The Delta state is characterized by synchronized slow waves, typically ranging from 0.5 to 4 Hz, during the deepest phase of non-REM sleep. These waves facilitate physical repair through the release of growth hormones, support immune function by regulating cytokines, and enable memory consolidation by coordinating communication between the hippocampus and cortex. Techniques like polysomnography and EEG help us measure the frequency, amplitude, and duration of these Delta waves. Key studies have shown that enhancing slow-wave activity—through methods like transcranial stimulation, acoustic phase-locking, or behavioral therapy—can restore deep sleep and improve cognitive and health outcomes.
Conditions such as insomnia and obstructive sleep apnea disrupt Delta sleep, reducing the secretion of growth hormones, impairing the clearance of neurotoxic proteins, and undermining declarative memory. Effective treatments, including CPAP, CBT-I, tDCS, and acoustic stimulation, can recover a significant portion of lost slow-wave sleep, thereby lowering inflammatory markers and improving daily performance.
In everyday life, maintaining a regular sleep schedule, reducing exposure to blue light in the evening, and managing stress can bolster deep sleep. Protecting Delta sleep enhances alertness, mood stability, and resistance to disease.
Looking ahead, research needs to focus on mapping the brain circuits that generate slow oscillations, understanding their interactions with other sleep rhythms, and developing safe pharmacological agents to enhance deep sleep without disrupting overall sleep structure. Long-term studies in aging and dementia populations will help determine whether targeted enhancement of Delta sleep can slow cognitive decline. By integrating personalized sleep profiles with tailored interventions, we can preserve deep sleep and support cognitive and physical health throughout life.
Just as ambient music creates a soothing atmosphere that can subtly influence our mood and relaxation, understanding and nurturing our Delta sleep can subtly yet profoundly impact our overall well-being. By paying attention to the rhythms and patterns of our sleep, we can create a harmonious environment for our bodies and minds to thrive.
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Further Reading
- Buzsáki, G. (2006). Rhythms of the Brain. Oxford University Press.
- Diekelmann, S., & Born, J. (2010). The memory function of sleep. Nature Reviews Neuroscience, 11(2), 114–126.
- Xie, L., et al. (2013). Sleep drives metabolite clearance from the adult brain. Science, 342(6156), 373–377.
