
Nurture your brain’s sleep evolution, don’t suppress it. You'll naturally sleep easier, deeper, and longer, if you do.
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From 10pm to 7am, your brain isn’t shutting down — it’s running the night shift of your life!
Millions of years of evolution have shaped the human brain to be most active when we think it’s asleep. Strange, but true.
Yet in today’s world, when sleep gets patchy or delayed, many Australians reach for chemical sedatives — medications that dampen brain activity and force it toward unconsciousness. But what if that very intense brain activity is the point of sleep?
New(ish) clinical research, powered by fMRI scanners that show real-time brain activity, reveals a startling truth: REM sleep is anything but restful for your brain. It’s emotionally intense, chemically rich, and absolutely necessary. And so is everything that happens before and after it — from 10pm right through the various phases of sleep to morning dawn. Below is a synopsis of what the brain does each 30 minutes between going to sleep at 10pm and waking up at 7am.
Read it through then ask yourself a question: Do you really think that hitting your brain with a "chemical hammer" to suppress nighttime activity in healthy adults is prudent, should you want your brain to stay sharp into old age?
10:00 PM – The down-regulation into early phases of sleep begins
You ease into Stage 1 sleep, also known as the hypnagogic transition. Neuronal firing begins to decouple between sensory and association areas. The lateral hypothalamus reduces orexin release, suppressing wake-promoting pathways. Vascular tone in the skin shifts, promoting conductive heat loss. Respiration slows as the medullary centres down regulate CO2 sensitivity. This is a fragile phase — external sounds or light can reverse it. Thermoreceptors in the pre-optic area of the hypothalamus monitor ambient temperature. If it's too high, the descent into deeper sleep halts. Melatonin, secreted by the pineal gland, continues to rise, signalling to peripheral clocks that systemic down-regulation is underway.
10:30 PM – Filtering out the noise
Stage 2 sleep locks in. Brainwaves produce sleep spindles and K-complexes — signals thought to gate sensory input at the thalamus. The baroreflex dampens cardiovascular activity, and core body temperature drops further, relieving the brain of thermal pressure. Autonomic tone shifts: parasympathetic dominance begins. CSF (fluid) movement initiates gently around the fourth ventricle — one of the brain’s central fluid reservoirs located near the brainstem. This early fluid circulation flows through narrow cerebral aqueducts and begins priming the ventricular system for the more vigorous fluid exchange that will come during deep sleep. Pressure gradients begin to build subtly between the ventricles and surrounding tissues, setting the stage for the glymphatic system's overnight "flushing" (clearance) mission.
11:00 PM – First deep clean
Stage 3, or slow-wave sleep (SWS), arrives. Neurons across the cortex begin firing in high-amplitude, low-frequency delta waves, coordinated by thalamocortical feedback loops. This synchrony enables efficient downscaling of synaptic potentiation — a form of neural housekeeping. At the same time, the glymphatic system activates: astrocytic endfeet open aquaporin-4 water channels, widening the perivascular space. Pulsatile arterial pressure from the Circle of Willis drives CSF through these interstitial pathways. Cellular waste — including tau and beta-amyloid proteins — begins clearing. Growth hormone, released from the anterior pituitary under hypothalamic control, supports tissue repair and glucose metabolism. The vagus nerve dominates autonomic tone, reducing cardiac output and gastrointestinal activity, shifting the body's resources inward.
11:30 PM – Deep sleep peaks
This is peak glymphatic "flushing" efficiency. Neuronal shrinkage increases extracellular space by up to 60%, reducing resistance to CSF flow. CSF enters via periarterial channels and is exchanged with interstitial fluid through aquaporin-4 water channels on astrocyte membranes. The movement of waste products toward the perivenous routes clears protein aggregates and metabolic debris. Systemic circulation stabilizes: blood pressure reaches its circadian nadir, and heart rate variability increases due to dominant parasympathetic tone. Hepatic (liver) metabolism of systemic waste products peaks in parallel. Brain glucose utilization drops, with neurons relying more on astrocyte-derived lactate. If core temperature begins rising — due to insulation (excessive bedding) or poor airflow — thermosensitive neurons in the hypothalamus may prompt a brief arousal.
12:00 AM – The dreams softly begin
REM sleep begins. Cortical activity accelerates into beta and gamma frequency ranges. The brainstem’s pontine tegmentum initiates muscle atonia via descending inhibitory projections to spinal motor neurons. Meanwhile, acetylcholine floods the cortex, while serotonin and norepinephrine release from the raphe nuclei and locus coeruleus halt. Visual association areas light up, enabling vivid dream imagery. The amygdala and anterior cingulate cortex become hyperactive, replaying emotional signals stored during the day. Thermoregulation is suspended — the hypothalamus no longer prompts sweating or shivering. The pre-Bötzinger complex adjusts respiratory rhythm to match dream scenarios. If temperature rises above a narrow comfort threshold or interstitial pressure increases from impaired (fluid) drainage, cortical arousal (awakening) may ensue.
12:30 AM – Intermission
You shift back into Stage 2 NREM. Thalamocortical circuits reduce their burst-firing activity. K-complexes reappear, transiently hyperpolarizing cortical neurons, potentially acting as a protective mechanism against awakening. Muscle tone returns modestly, and respiratory rate stabilizes. CSF (fluid) pulsation resumes in the ventricular system, aided by the flexing of arterial walls and the rebound of venous sinus pressure. Baroreceptor input modulates cardiac rhythm to stabilize perfusion. This phase serves as a metabolic reset point before deeper processing resumes. If fluid balance or thermal regulation deviates, micro-awakenings may occur without conscious recall.
1:00 AM – The second flush
You re-enter Stage 3 slow-wave sleep. Cortical neurons hyperpolarise, creating large amplitude delta oscillations. Glymphatic flow intensifies, targeting the medial temporal lobes and hippocampus. Perivascular spaces open wider due to astrocytic modulation of aquaporin-4 channels. During this phase, sharp-wave ripples from the hippocampus coordinate with thalamic sleep spindles and cortical slow oscillations — synchronised patterns believed to underlie memory consolidation. Growth hormone pulses stimulate somatic repair, while glucose transport is temporarily reduced to favor lactate-fueled neural metabolism. Any disruption to these tightly timed bioelectrical and hydraulic processes — from overheating to dehydration — threatens the night's cleanup.
1:30 AM – Emotional REM
Another REM period begins — longer than the last. Cortical desynchrony returns as high-frequency waves dominate EEG patterns. Activity in the amygdala, hippocampus, and anterior cingulate cortex surges, coordinating with cholinergic input from the basal forebrain. These emotional networks reactivate stored affective experiences and initiate memory reconsolidation. CSF (fluid) flow through the glymphatic channels diminishes significantly, as REM physiology favours localised metabolic bursts over fluid exchange. Respiratory variability is governed by brainstem circuits responsive to dream-related imagery. Thermoregulation is silenced. If your ambient environment is too warm or if unresolved cognitive/emotional loads remain, arousal thresholds drop — often culminating in premature awakening or fragmented sleep.
2:00 AM – Floating lightly
You cycle into NREM Stage 2. The thalamus reasserts control over sensory input, gating signals through inhibitory interneurons. EEG reveals spindles modulated by GABAergic cells in the reticular nucleus. Meanwhile, baroreflex sensitivity is restored, modulating autonomic balance as cardiac variability stabilizes. CSF (fluid) pulses lightly between lateral brain ventricles, with minor redistribution of intracranial volume as blood shifts in response to pressure gradients. The hypothalamus monitors vasopressin and aldosterone levels, maintaining water reabsorption and osmolality. Even minor dehydration or circulatory inefficiency at this point can generate homeostatic error signals that trigger transient cortical arousal (awakening).
2:30 AM – The vulnerable wake-up window
REM returns. By now, cortisol levels begin their pre-dawn ascent, driven by activation of the HPA axis and stimulation of CRH and ACTH. For older adults or those with shallow prior sleep, this circadian hormonal transition becomes destabilising. If earlier movement of glymphatic fluids failed to sufficiently clear metabolic waste, neuroinflammatory markers rise, subtly impairing synaptic function and increasing arousability. The anterior insula, sensitive to interoception, may detect bladder pressure, cardiac shifts, or subtle thermal gradients. Combined with reduced melatonin and suppressed thermoregulation, this makes 2:30 AM one of the most common spontaneous wake-up points of the night.
3:00 AM – Teetering between sleep and stirring
Melatonin synthesis winds down as exposure to even trace amounts of light begins resetting the SCN (circadian) clock. Cortisol secretion via the HPA axis ramps up, stimulating gluconeogenesis in the liver and promoting alertness. Locus coeruleus neurons begin firing again, reintroducing norepinephrine into the cortical landscape. The salience network — especially the anterior insula and dorsal anterior cingulate cortex — shows increasing synchrony, scanning for changes in internal and external conditions. Cerebral perfusion increases slightly, raising baseline activity levels. If thermoregulation remains suppressed and the cardiovascular system senses any shift in posture, pressure, or temperature, the RAS (reticular activating system) can trigger preconscious arousal. This is the moment when a single thought, noise, or discomfort can derail sleep.
3:30 AM – REM, again
This REM phase is frequently the most emotionally charged. Cortical theta-gamma coupling enhances synaptic plasticity in prefrontal-limbic circuits. The amygdala, hippocampus, and medial prefrontal cortex engage in high-volume emotional data exchange. Vivid dream content often emerges as a result of this cross-talk. The locus coeruleus remains inhibited, allowing uninterrupted visual and emotional integration. Brainstem cholinergic neurons maintain cortical activation, while REM-on GABAergic neurons enforce muscle atonia. The body cannot thermoregulate, so environmental heat buildup subtly stresses the system. The longer this REM period is allowed to run, the more effectively emotional conflicts and memory fragments from the prior day are restructured — but it is also when sleep is most vulnerable to disruption from external or internal imbalance.
4:00 AM – Fragile stillness
You enter light NREM sleep, predominantly Stage 2. EEG shows intermittent spindles and occasional K-complexes as the brain toggles between maintaining unconsciousness and prepping for reactivation. Autonomic function begins its transition: heart rate and blood pressure creep upward, guided by early morning sympathetic tone. AVP (arginine vasopressin) still suppresses nocturnal urine production, but its influence wanes. The bladder stretches, stimulating pelvic afferents that activate the pontine micturition center. Meanwhile, vestibular and proprioceptive feedback from minor movements may stimulate cortical regions in lighter sleepers. If thermal load has accumulated due to poor ventilation or excessive insulation, hypothalamic thermosensors become sensitized, raising the risk of spontaneous wakefulness.
4:30 AM – One more intense dream
A final REM burst begins — typically the longest and most metabolically active. Glucose uptake spikes in the occipital and limbic regions. The brain’s temperature reaches its peak, driven by dense regional activation and suppressed thermolytic feedback. Acetylcholine floods the forebrain, keeping cortical neurons in a high-frequency firing state. The default mode network re-engages, linking together fragmented memories from earlier REM cycles. The PFC remains partially disengaged, which is why dreams may feel vivid but illogical. If glymphatic drainage was successful earlier, astrocytic swelling has subsided, allowing clear signaling. If not, intracranial pressure or residual metabolic waste may create subtle discomfort, increasing the chance of premature arousal.
5:00 AM – Light sleep, light touch
Stage 1 reappears as a bridge to waking. Thalamocortical connectivity resumes, increasing responsiveness to environmental cues. The brain's arousal systems — including the RAS and basal forebrain — begin ramping up, quietly preparing the cortex to reboot. Sympathetic tone increases, promoting adrenal activity and elevating resting heart rate. Cortisol nears its zenith. If previous sleep cycles were truncated or fragmented, this transition can feel jarring, leading to morning grogginess or sleep inertia. If preserved, this fragile phase sets the stage for one final REM flourish.
5:30 AM – Final REM, final sweep
The final REM stage is a sweeping neurological clean-up. Cortical regions involved in executive function — such as the dorsolateral prefrontal cortex — begin re-engaging. The hippocampus and default mode network coordinate to finalise the emotional and procedural sorting of recent memories. Gamma bursts signal the consolidation of long-term learning. This is the apex of dream richness and emotional recalibration. Meanwhile, cortisol release peaks, priming metabolism, inflammation control, and blood glucose. Successful navigation through this stage correlates with enhanced psychological resilience and emotional adaptability during the day.
6:00 AM – Almost there, as the sun rises
Your hypothalamus begins orchestrating the transition to wakefulness. The suprachiasmatic nucleus (SCN) primes sympathetic reactivation, while thermoregulation resumes — now capable of initiating shivering or sweating responses again. Blood pressure rises due to the early-morning surge of angiotensin II and cortisol. The pineal gland ceases melatonin secretion. REM fragments may still be active at the edges of consciousness, leading to half-dreaming states. Visual sensitivity increases as the retina begins responding to light more acutely, prompting early-stage recalibration of circadian input. If prior sleep was disrupted or REM was insufficient, cortisol may spike prematurely, impacting mood, hunger, and immune response throughout the day.
6:30 AM – Mind on the edge
Melatonin has been suppressed completely. The SCN (circadian clock) aligns tightly with first light, anchoring the next circadian cycle. The default mode network remains active, and fleeting REM imagery may still ripple through prefrontal circuits. This is why dreams — and nightmares — are often remembered during this phase: the dorsolateral prefrontal cortex re-engages just in time to archive the tail end of REM sequences. These last dreams are not always random. Many contain thematic fragments of recent or older memories, reorganised by emotional salience. The brain is deleting the mundane and re-tagging high-impact experiences. In doing so, it’s preserving key emotional markers and discarding mental clutter to make room for today’s new learning.
7:00 AM – Wake up, not shut down
Cortisol peaks sharply, driving final arousal as the hypothalamic-pituitary-adrenal (HPA) axis reaches full activation. Your renal, digestive, and endocrine systems reengage: pancreatic insulin sensitivity rises, gastrointestinal motility resumes, and the adrenal cortex finalises its hormonal morning cocktail. The glymphatic system — having completed its nighttime drainage of interstitial waste — goes dormant, awaiting the next sleep cycle.
The reticular activating system (RAS) sends ascending cholinergic projections to fully awaken the cortex. Meanwhile, the default mode network retracts as task-positive networks come online. If the final REM phase completed without interruption, your brain has just finished re-archiving long-term memories, discarding emotional noise, and updating behavioural strategies based on recent experiences.
If dreams or nightmares linger in your awareness, they are often fragments of older, emotionally tagged memories that were reorganised just before waking — a final neurological filing process that deletes the irrelevant and keeps what still matters.
Waking up now isn’t a reboot. It’s a seamless continuation — the cognitive version of surfacing from deep water, with clarity, calm, and readiness.
References:
Brain Activity During Sleep (10 PM – 7 AM): Key Physiological Processes and Evidence
1. REM and Deep Sleep: Memory Consolidation, Emotional Processing, and Glymphatic Clearance
- Fultz et al. (2019) – Using fast MRI in sleeping humans, this study found that the slow electrical brain waves of non-REM deep sleep (linked to memory consolidation) are tightly coupled with large oscillating waves of cerebrospinal fluid (CSF) flow, which help clear metabolic waste pubmed.ncbi.nlm.nih.gov. In other words, during deep slow-wave sleep the brain appears to simultaneously reinforce memories and flush out toxins via the “glymphatic” system. Fultz, N. E., et al. (2019). “Coupled electrophysiological, hemodynamic, and cerebrospinal fluid oscillations in human sleep.” Science, 366(6465): 628–631.* (PubMed)
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Kumar et al. (2020) – In a mouse experiment, researchers showed that REM sleep is causally required for certain types of memory consolidation. They tracked newly formed neurons in the hippocampus and found these cells reactivated during REM after a learning task. Silencing this activity during REM (via optogenetics) impaired the strengthening of the fear memory, indicating that REM sleep neuronal activity is crucial for consolidating episodic (especially emotional) memories pubmed.ncbi.nlm.nih.gov. Kumar, D., et al. (2020). “Sparse activity of hippocampal adult-born neurons during REM sleep is necessary for memory consolidation.” Neuron, 107(3): 552–565.e10.* (PubMed)
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Wassing et al. (2019) – This clinical study linked REM sleep continuity with next-day emotional regulation. It found that when REM sleep was highly fragmented (“restless REM”), participants failed to show the normal overnight reduction in amygdala reactivity to prior emotional stress. By contrast, longer, uninterrupted REM bouts were associated with a greater drop in amygdala activity and negative emotion by morning pubmed.ncbi.nlm.nih.gov. Experimentally inducing cues during REM confirmed that consolidated REM helps the brain to process emotional experiences, whereas disrupted REM leaves emotional distress largely “undissolved” pubmed.ncbi.nlm.nih.gov. Wassing, R., et al. (2019). “Restless REM sleep impedes overnight amygdala adaptation.” Current Biology, 29(14): 2351–2358.e4.* (PubMed)
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Toh et al. (2025) – A human neuroimaging study in older adults tied sleep quality, glymphatic clearance, and memory together. It used MRI measures of glymphatic function (CSF–fluid transport) and found that poorer sleep (more disturbances) was associated with reduced glymphatic flow and weaker brain network connectivity, which in turn correlated with memory declines on cognitive tests. In “good sleepers,” better glymphatic function was linked to stronger brain network coupling and memory performance, whereas this brain-cleaning and memory network link was disrupted in “poor sleepers” nature.com. This provides evidence that healthy deep sleep supports both effective waste clearance and memory maintenance as we age. Toh, C. H., et al. (2025). “Effects of sleep on the glymphatic functioning and multimodal human brain network affecting memory in older adults.” Molecular Psychiatry, 30: 1717–1729.* (Nature)
2. Sedatives’ Impact on REM, Slow-Wave Sleep, and Related Physiology
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de Mendonça et al. (2023) – This systematic review of clinical trials confirms that benzodiazepine sedatives markedly alter normal sleep architecture. Across studies, benzodiazepines (prescribed for insomnia) were found to increase light NREM stage-2 sleep while significantly suppressing deep slow-wave sleep (stages 3–4) and REM sleep during the night pubmed.ncbi.nlm.nih.gov. In short, these drugs produce “lighter” sleep at the expense of the restorative stages. The authors note that such shifts in sleep stages may lead to deficits in daytime concentration and working memory as a consequence pubmed.ncbi.nlm.nih.gov. de Mendonça, F. M. R., et al. (2023). “Benzodiazepines and sleep architecture: A systematic review.” CNS & Neurological Disorders – Drug Targets, 22(2): 172–179.* (PubMed)
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Simon et al. (2022) – This placebo-controlled sleep lab study examined the popular Z-drug zolpidem and found it also alters sleep stages, albeit in a somewhat different way. Zolpidem (10 mg) increased the duration of slow-wave (deep) sleep and increased fast sleep spindles, but it significantly reduced total REM sleep time compared to natural sleep link.springer.com. Notably, the zolpidem nights preserved memory for negative emotional information better than placebo (the drug prevented the normal forgetting of upsetting images), suggesting that pharmacologically induced sleep can modulate memory processing differently than natural sleep link.springer.comlink.springer.com. Simon, K. C., et al. (2022). “Zolpidem maintains memories for negative emotions across a night of sleep.” Affective Science, 3: 389–399.* (Springer Open)
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Hauglund et al. (2025) – This neuroscience study highlights how sedative-induced sleep may omit critical physiological rhythms. Using mice, the authors showed that natural NREM sleep features slow oscillations in norepinephrine levels and blood flow that drive rhythmic CSF movements; these pulses act like a pump to flush out brain waste. When mice were given the sedative zolpidem, it “knocked them out” but suppressed these normal norepinephrine oscillations and the associated CSF flow, thereby disrupting the brain’s nightly waste-clearance process pubmed.ncbi.nlm.nih.gov. This finding underscores that drug-induced sleep is not equivalent to natural sleep – some deep restorative processes (like glymphatic cleansing) may be impaired under common sleeping pills pubmed.ncbi.nlm.nih.gov. Hauglund, N. L., et al. (2025). “Norepinephrine-mediated slow vasomotion drives glymphatic clearance during sleep.” Cell, 188(3): 606–622.e17.* (PubMed)
3. Thermoregulation, CSF Dynamics, and Nocturnal Awakenings
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Okamoto-Mizuno & Mizuno (2012) – This review explains that the sleep environment’s temperature has a profound effect on sleep continuity. In real-life conditions (with typical bedding), an overly warm ambient temperature causes more frequent awakenings and arousals at night, while also reducing time spent in slow-wave and REM sleep jphysiolanthropol.biomedcentral.com. In contrast, mild cooling tends to deepen sleep. Excess humidity plus heat further increases wake-ups. These findings show that failing to dissipate body heat can trigger cortical arousals and fragments sleep, underlining the importance of thermal regulation for staying asleep jphysiolanthropol.biomedcentral.com. Okamoto-Mizuno, K., & Mizuno, K. (2012). “Effects of thermal environment on sleep and circadian rhythm.” Journal of Physiological Anthropology, 31(1): 14.* (BioMed Central)
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Ancoli-Israel et al. (2011) – This paper focused on nocturia (excessive nighttime urination) as a trigger for sleep disturbance. It highlights that nocturia is a very common cause of awakenings from sleep and is associated with significantly impaired sleep quality and daytime functioning when frequent pubmed.ncbi.nlm.nih.gov. Individuals who have to get up two or more times per night to void report much more sleep disruption and “bother.” The authors argue that nocturia should be recognized as an important target for intervention, since these hydration-related awakenings fragment sleep and can lead to chronic sleep loss and its health consequences pubmed.ncbi.nlm.nih.gov. Ancoli-Israel, S., et al. (2011). “The effect of nocturia on sleep.” Sleep Medicine Reviews, 15(2): 91–97.* (PubMed)
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Hauglund et al. (2025) – In the context of normal sleep, this study noted that the brain periodically creates brief “micro-arousals” during deep NREM sleep which are tied to surges in norepinephrine and blood vessel pulsing eurekalert.org. These subtle cortical arousals (lasting only seconds) trigger waves of CSF through the brain and are thought to be critical for nightly brain maintenance (helping pump out waste) eurekalert.org. Such micro-arousals do not usually reach full awakening, but they represent an intrinsic mechanism by which internal dynamics (neuromodulator bursts, vasomotion) can momentarily lighten sleep. This suggests that some nocturnal arousals are endogenously generated by the brain for housekeeping purposes, distinguishing them from external disturbances. Hauglund, N. L., et al. (2025). “Norepinephrine-mediated slow vasomotion drives glymphatic clearance during sleep.” Cell, 188(3): 606–622.e17.* (PubMed)
4. Long-Term Effects of Suppressing Natural Sleep Architecture via Sedatives (Cognitive & Emotional)
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Tseng et al. (2020) – A large cohort study in Taiwan (n > 260,000) found a strong association between long-term sedative use and dementia risk. Older adults who regularly used benzodiazepines or Z-hypnotics had significantly higher odds of developing dementia over ~8 years of follow-up compared to non-users. In particular, short-acting benzodiazepines and Z-drugs were associated with a ~1.8–2.0-fold increase in dementia risk, even after adjustments pubmed.ncbi.nlm.nih.gov. Taking multiple sedatives concurrently further amplified the risk. These findings underline concerns that chronic use of sleep medications may contribute to long-term cognitive decline and dementia, possibly by interfering with normal restorative sleep processes pubmed.ncbi.nlm.nih.gov. Tseng, L. Y., et al. (2020). “Benzodiazepines, Z-hypnotics, and risk of dementia: special considerations of half-lives and concomitant use.” Neurotherapeutics, 17(1): 156–164.* (PubMed)
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Hauglund et al. (2025) – Beyond acute effects, this neuroscientific study raised a red flag about potential long-term brain consequences of habitual sedative use. As noted, zolpidem-induced sleep in mice lacked the normal CSF cleaning pulses; the glymphatic “brain-washing” function was suppressed by the drug, which could allow toxic proteins to accumulate over time eurekalert.org. The authors caution that long-term reliance on such sleep aids might increase vulnerability to neurodegenerative diseases like Alzheimer’s, essentially by chronically short-circuiting the brain’s overnight maintenance processes eurekalert.orgeurekalert.org. This work suggests that preserving natural sleep architecture (with its cycles of REM and deep sleep) is vital for cognitive health in the long run. Hauglund, N. L., et al. (2025). “Norepinephrine-mediated slow vasomotion drives glymphatic clearance during sleep.” Cell, 188(3): 606–622.e17.* (Cell Press)
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Liu et al. (2020) – A systematic review and meta-analysis examined the cognitive effects of long-term benzodiazepine use in older adults. It found that even in elders without dementia, chronic BZD users perform worse on certain cognitive tests than non-users. Notably, processing speed was significantly reduced in regular BZD users (e.g. lower digit-symbol substitution test scores) frontiersin.org. In cases of benzodiazepine abuse (very prolonged or high-dose use), users also showed mild declines in global cognition (Mini-Mental State Exam) compared to controls frontiersin.org. These findings reinforce that long-term use or overuse of sedative-hypnotics can lead to persistent cognitive impairments, even if overt dementia is not present. Liu, L., et al. (2020). “The effects of benzodiazepine use and abuse on cognition in the elders: a systematic review and meta-analysis.” Frontiers in Psychiatry, 11: 755. (Frontiers)