Sleep, Mood, and Cognitive Vulnerability Beyond 50
Ask most people over 50 how they are sleeping and the answer is rarely straightforward. Too light. Waking at 3am. Taking an hour to drop off. Feeling unrested despite spending eight hours in bed. Running on less than you used to. Accepting it, because what else is there to do.
The acceptance is understandable. The resignation is not.
Poor sleep in midlife and later life is not simply a quality-of-life inconvenience. It is one of the most significant and modifiable risk factors for depression, anxiety, and cognitive decline that we know of, and one of the most undertreated. The research on the sleep-mood-brain connection after 50 is striking in both its clarity and its implications: what happens in the sleeping brain has consequences that reach deep into waking life, and those consequences accumulate over time.
This article explains what the research tells us about sleep after 50, how it changes, why those changes matter, and what the evidence says can genuinely help.
The sleep problem nobody talks about honestly
There is a cultural tendency to normalise poor sleep in midlife and later life in a way that would not be acceptable for any other health concern. We would not casually accept persistent pain, persistent low mood, or persistent breathlessness as an inevitable feature of getting older. Yet disrupted sleep is routinely shrugged off as something to manage around rather than address.
Part of this is because sleep problems are so common. A 2017 report found that approximately 33–45% of Australian adults report inadequate sleep, with rates increasing significantly from midlife onward (Adams et al., 2017). When something affects nearly half the population, it can start to feel normal — even when the consequences are anything but.
Part of it is also that sleep problems in later life present differently from younger-adult insomnia and are sometimes harder to identify and treat. But harder is not the same as impossible. And the case for treating sleep problems in midlife and later life, rather than managing around them, is one of the strongest in preventive mental health and brain health research.
How sleep changes after 50, and why
Understanding why sleep changes with age is the foundation for understanding what can be done about it. Several distinct mechanisms are involved.
Architecture shifts
Sleep is not a uniform state. It cycles through distinct stages (light sleep, deep slow-wave sleep, and REM sleep) in patterns that repeat across the night. The distribution of these stages changes with age in ways that are clinically meaningful.
Deep slow-wave sleep — the most restorative phase, during which the body repairs tissue, consolidates memories, and clears metabolic waste from the brain — decreases substantially with age. A 2021 review by Scullin and Bliwise found that slow-wave sleep declines by approximately 2% per decade from early adulthood, with the most pronounced changes occurring between the forties and sixties (Scullin & Bliwise, 2021). The result is that even people who spend adequate time in bed may be getting substantially less of the sleep that is most restorative.
Circadian rhythm changes
The body’s internal clock, known as the circadian rhythm, shifts with age in a direction called phase advancement: older adults tend to feel sleepy earlier in the evening and wake earlier in the morning. This is a biological change, not a lifestyle choice, and it can create significant misalignment between when a person’s body wants to sleep and when their life, whether social, family, or work for example, actually allows it. The result is often a compression of sleep opportunity that leaves people both tired and frustrated.
Menopause and sleep
For women, the hormonal changes of perimenopause and menopause have a direct and well-documented effect on sleep quality. Hot flashes and night sweats disrupt sleep continuity; declining oestrogen affects the regulation of sleep architecture; and the mood symptoms frequently associated with the menopausal transition — particularly anxiety and depression — independently worsen sleep. A 2020 review by Jehan et al. found that sleep disturbance was reported by 39–47% of perimenopausal women and up to 60% of postmenopausal women, making it one of the most prevalent and impactful symptoms of the menopausal transition (Jehan et al., 2020).
Sleep apnoea
Obstructive sleep apnoea — the repeated partial or complete blockage of the airway during sleep — becomes substantially more common with age, affecting an estimated 30–80% of older adults depending on diagnostic criteria (Young et al., 2002). It is a major but frequently undiagnosed cause of disrupted sleep, daytime fatigue, mood disturbance, and — as the evidence increasingly shows — accelerated cognitive decline and cardiovascular risk. Its presence should be considered in any older adult presenting with unexplained fatigue, mood problems, or cognitive concerns.
Sleep and mood: a two-way relationship
The relationship between sleep and mood is not one-directional. Poor sleep worsens mood, and poor mood worsens sleep — a cycle that can become self-sustaining and increasingly difficult to interrupt without deliberate intervention.
Sleep loss and depression
The link between sleep disturbance and depression is one of the most robust findings in psychiatry. A 2020 meta-analysis by Baglioni et al. found that insomnia approximately doubles the risk of developing depression — a finding consistent across age groups and geographic contexts (Baglioni et al., 2020). Critically, this relationship is bidirectional: sleep disturbance is both a symptom of depression and a cause of it, meaning that treating sleep is not merely addressing a symptom — it is potentially interrupting the pathway to depression itself.
In older adults, the relationship between sleep and depression has additional dimensions. Late-life depression frequently presents with prominent sleep disturbance — particularly early morning waking — and sleep problems in this age group are among the most reliable predictors of depression onset and recurrence. A 2022 study by Ge et al. found that poor sleep quality was significantly associated with both the incidence and severity of depression in adults over 60, with the association stronger in those with fewer social connections and lower levels of physical activity (Ge et al., 2022).
Sleep loss and anxiety
The relationship between sleep and anxiety is equally well-established and operates through similar bidirectional mechanisms. Anxiety disrupts sleep — through rumination, physiological arousal, and the mind’s tendency to use the quietness of night as an opportunity to process worry. And poor sleep amplifies anxiety — through a reduction in the brain’s capacity to regulate emotional responses and a lowering of the threshold at which ordinary stressors feel overwhelming.
A 2019 study by Simon and Walker found that even a single night of sleep deprivation significantly increased anticipatory anxiety in healthy adults, and that this effect was driven by heightened activity in the brain’s threat-detection system (Simon & Walker, 2019). In people who are already anxious, chronic sleep disruption creates a continuous state of emotional vulnerability that makes anxiety harder to manage and harder to treat.
The emotional amplification effect
One of the most important findings in recent sleep research is what neuroscientists call emotional amplification: the finding that sleep-deprived brains respond to emotional stimuli — both negative and positive — with substantially greater intensity than well-rested brains. A 2021 review by Walker found that sleep deprivation increased activity in the brain’s emotional alarm centre by up to 60%, while simultaneously reducing the regulatory influence of the prefrontal cortex (Walker, 2021).
In practical terms, this means that poor sleep does not just make people feel worse — it fundamentally alters how they process emotional experience. Irritability, emotional overwhelm, catastrophic thinking, and difficulty recovering from setbacks are not personality traits or signs of weakness. In many cases, they are the predictable consequences of a brain that is not getting adequate sleep.
Sleep and cognitive vulnerability: what the brain needs at night
Beyond its effects on mood, sleep plays a specific and critical role in brain health — a role whose full significance has only become clear in the past decade.
Memory consolidation
During sleep — particularly during slow-wave sleep and REM sleep — the brain engages in active memory processing: transferring information from short-term storage to long-term memory, strengthening important connections, and pruning those that are no longer needed. This process is not passive storage. It is active reconstruction, and it is essential for the kind of learning, recall, and cognitive flexibility that people notice most when it begins to decline.
A 2014 study by Diekelmann found that sleep-dependent memory consolidation is significantly impaired by both reduced sleep duration and disrupted sleep architecture — and that these impairments accumulate over time in ways that are not fully reversed by a single night of recovery sleep (Diekelmann, 2014). The cognitive effects of chronic poor sleep are therefore not simply the result of last night’s disruption — they are the cumulative product of months or years.
Glymphatic clearance and dementia risk
One of the most significant discoveries in neuroscience in the past decade is the glymphatic system: a network of channels in the brain that, during deep sleep, expands to allow cerebrospinal fluid to flush out metabolic waste products — including proteins most closely associated with Alzheimer’s disease.
This process occurs primarily during slow-wave sleep and is substantially impaired by sleep disruption. A landmark study by Xie et al. found that even a single night of sleep deprivation was associated with a measurable increase in the accumulation of these proteins in the human brain — suggesting that the glymphatic system’s clearance function is acutely sensitive to sleep loss (Xie et al., 2013). The implication is stark: chronic poor sleep may not merely be associated with dementia risk — it may directly contribute to the biological processes that underlie it.
What the long-term data shows
The long-term epidemiological data is consistent with this mechanistic picture. A landmark 2021 study by Sabia et al., tracking over 7,000 adults for 25 years, found that consistently sleeping six hours or fewer per night at age 50 was associated with a 30% higher risk of developing dementia in later life, independent of other health and lifestyle factors (Sabia et al., 2021). This finding has been widely replicated and is now included in the dementia prevention evidence base in the 2024 Lancet Commission report (Livingston et al., 2024).
What makes these findings both sobering and important is that they point to something modifiable. Sleep is a risk factor that responds to intervention in a way that many biological risk factors for dementia do not.
Subjective sleep, objective sleep, and the anxiety loop
A complicating feature of sleep problems in midlife and later life is the frequent mismatch between how people experience their sleep and what objective measurement of their sleep actually shows. Many people who report sleeping poorly — waking frequently, lying awake for hours, feeling unrested — show, on objective sleep monitoring, less disruption than they perceive.
This is not a reason to dismiss their experience. Subjective sleep quality — how rested people feel, how much they worry about sleep, and how much distress their sleep causes — is independently associated with mental health and wellbeing outcomes, regardless of what objective measurement shows (Kyle et al., 2020). A person who sleeps six hours but feels they have slept well fares better than a person who sleeps six hours but is convinced they have barely slept at all.
This discrepancy matters clinically because it points to a psychological maintaining factor that is distinct from the sleep problem itself: sleep-related anxiety. Many people with insomnia develop a secondary preoccupation with sleep — monitoring it, catastrophising about its consequences, and approaching bedtime with dread — that independently maintains and amplifies the insomnia. This pattern is one of the central targets of Cognitive Behavioural Therapy for Insomnia (CBT-I), and its presence is not a sign that the sleep problem is less real — it is a sign that psychological treatment is particularly indicated.
What makes sleep harder to treat in midlife and later life, and what doesn’t
It is sometimes assumed that sleep problems in older adults are inherently less responsive to treatment — that the biological changes of ageing make intervention less effective. The evidence does not support this view.
A 2019 meta-analysis by Geiger-Brown et al. found that Cognitive Behavioural Therapy for Insomnia (CBT-I) was effective for insomnia in older adults, with effect sizes comparable to those seen in younger populations, and that these effects were maintained at follow-up (Geiger-Brown et al., 2019). Older adults, as with anxiety treatment, tend to be motivated and engaged treatment participants.
What does require adaptation is attention to the specific causes and contexts of sleep disruption in this age group: the potential role of sleep apnoea, the effects of menopause, the contribution of pain and other physical health conditions, the sleep-disrupting effects of certain medications, and the bidirectional relationship with mood disorders that may need to be addressed concurrently. A skilled clinician treats the sleep problem in the context of the whole person, not just as an isolated symptom.
What actually helps: the evidence
Cognitive Behavioural Therapy for Insomnia
Cognitive Behavioural Therapy for Insomnia (CBT-I) is the most evidence-based treatment for chronic insomnia across all age groups, and is recommended as first-line treatment over sleep medication by clinical guidelines including those of the American Academy of Sleep Medicine and the Australian Sleep Health Foundation. A 2019 meta-analysis by Zachariae et al. found that CBT-I produced significant and durable improvements in sleep onset latency, total sleep time, sleep efficiency, and subjective sleep quality, with effects maintained at long-term follow-up (Zachariae et al., 2019).
CBT-I works through several mechanisms: stimulus control (rebuilding the association between bed and sleep); sleep restriction (temporarily compressing sleep opportunity to consolidate sleep drive); cognitive restructuring (examining and shifting the beliefs and catastrophic thinking that maintain sleep anxiety); and relaxation techniques. It is delivered over six to eight sessions and can be conducted effectively via telehealth.
Crucially, CBT-I does not simply teach better sleep habits. It addresses the psychological maintaining factors, particularly sleep-related anxiety and unhelpful beliefs about sleep, which keep insomnia going long after its original trigger has resolved.
Sleep hygiene: useful but not sufficient alone
Sleep hygiene advice encompassing consistent wake times, limiting caffeine, avoiding screens before bed, maintaining a cool and dark room, is widely known and genuinely useful as a foundation. However, the research consistently shows that sleep hygiene alone is insufficient for established insomnia. A 2021 review by Chung et al. found that sleep hygiene education without accompanying behavioural and cognitive components produced only modest and short-lived improvements in insomnia severity (Chung et al., 2021). It is a necessary but not sufficient component of effective treatment.
Managing anxiety and depression
Because of the bidirectional relationship between sleep, mood, and anxiety, treating sleep in isolation is often not enough. For many people, anxiety and depression are significant contributors to their sleep disruption, and addressing them — through CBT, ACT, or other evidence-based approaches — is an essential part of improving sleep. Conversely, improving sleep typically produces meaningful improvements in mood and anxiety, making sleep treatment a valuable component of broader mental health intervention.
Physical activity
Regular physical activity is one of the most robustly supported behavioural interventions for sleep quality in older adults. A 2021 meta-analysis by Vanderlinden et al. found that aerobic exercise significantly improved subjective sleep quality, sleep duration, and sleep efficiency in adults over 50, with effects particularly strong for those with the most disrupted sleep at baseline (Vanderlinden et al., 2021). The mechanisms include the regulation of circadian rhythms, reduction of anxiety and depressive symptoms, and the promotion of deeper slow-wave sleep.
Alcohol: a sleep disruptor in disguise
Alcohol is one of the most common self-prescribed sleep aids in midlife and later life — and one of the most counterproductive. While alcohol facilitates sleep onset, it disrupts sleep architecture: increasing light sleep, suppressing slow-wave sleep and REM sleep, and producing a rebound effect in the second half of the night that results in early waking, fragmented sleep, and morning anxiety. A 2020 review by Park et al. found that habitual alcohol use was significantly associated with poorer sleep quality and greater sleep fragmentation in adults over 50, with effects worsening with increasing consumption (Park et al., 2020).
Medication: what to know
Sleep medications, including benzodiazepines and Z-drugs such as zolpidem, are widely prescribed for insomnia in older adults, but their use carries significant risks in this age group, including falls, cognitive impairment, dependency, and rebound insomnia on discontinuation. A 2021 review by Glass et al. found that sedative hypnotics in older adults were associated with a nearly five-fold increase in falls and fractures, substantially outweighing their modest benefits for sleep (Glass et al., 2021). Clinical guidelines consistently recommend CBT-I as first-line treatment and medication as a short-term adjunct at most.
If you are currently using sleep medication and want to reduce or stop, a GP or clinical psychologist can help you do this safely, and CBT-I has been shown to be effective in supporting medication discontinuation in older adults.
Frequently asked questions
Is poor sleep after 50 just a normal part of ageing?
Although it is widely recognised that sleep changes with age, poor sleep is not an inevitable or acceptable consequence of those changes. The changes in sleep architecture described above explain why sleep often feels lighter and more fragmented after 50, but they do not explain or excuse clinically significant insomnia, daytime fatigue, or mood disruption that significantly affects quality of life. These are treatable conditions, not facts of ageing. The assumption that they are normal is one of the primary reasons they go untreated.
How much sleep do I actually need after 50?
The evidence supports seven to eight hours as the optimal range for adults of all ages, including those over 50. A 2015 consensus statement by the American Academy of Sleep Medicine, based on a systematic review of the evidence, recommended seven to nine hours for adults and found that both short sleep (under six hours) and long sleep (over nine hours) were associated with adverse health outcomes (Hirshkowitz et al., 2015). The idea that older adults need less sleep is not well-supported by the evidence. What changes is sleep capacity or the ability to achieve adequate sleep; not sleep need.
Can poor sleep cause depression, or does depression cause poor sleep?
Both. And this is clinically important. A 2020 meta-analysis found that insomnia approximately doubles the risk of developing depression (Baglioni et al., 2020), meaning that poor sleep is a causal risk factor for depression, not merely a symptom of it. At the same time, depression is one of the most common causes of sleep disruption. This bidirectional relationship means that treating one without addressing the other often produces incomplete results, and that treating both together is generally more effective than treating either in isolation.
Does poor sleep really increase dementia risk?
Yes. And the evidence is increasingly clear on this. A 2021 study by Sabia et al. found that consistently sleeping six hours or fewer at age 50 was associated with a 30% higher risk of dementia in later life (Sabia et al., 2021). The mechanism involves the glymphatic system (the brain’s nocturnal waste-clearance process) which is substantially impaired by sleep loss, leading to the accumulation of proteins associated with Alzheimer’s disease. Sleep disruption is now included as a modifiable dementia risk factor in the 2024 Lancet Commission report (Livingston et al., 2024).
I’ve tried sleep hygiene and it doesn’t work. What else is there?
CBT-I is one option, and it is more effective than sleep hygiene alone. Sleep hygiene is a useful foundation but is insufficient for established insomnia on its own (Chung et al., 2021). CBT-I addresses the psychological maintaining factors such as sleep-related anxiety, unhelpful beliefs about sleep, stimulus control. It is delivered over six to eight sessions, can be conducted via telehealth, and has effects that are maintained long-term in a way that medication generally is not. A clinical psychologist trained in CBT-I is the appropriate person to deliver it.
How can a psychologist help with sleep problems?
A clinical psychologist can assess the full picture of your sleep, including the role of anxiety, depression, sleep-related beliefs and behaviours, and lifestyle factors, and offer CBT-I as the primary evidence-based treatment. Where anxiety or depression are significant contributors, these can be addressed concurrently using CBT, ACT, or other evidence-based approaches. At Upside Stories, sleep problems are treated in the context of the whole person and their broader mental health, rather than as an isolated complaint.
For those with significant cognitive health concerns, sleep treatment is also an important component of the Healthy Brain Happy Heart program, which addresses modifiable dementia risk factors including sleep, anxiety, physical activity, and social connection.
Do I need a GP referral to see a psychologist at Upside Stories?
No referral is needed to book. If you have a GP referral with a Mental Health Treatment Plan, Medicare rebates apply, reducing the cost of sessions significantly. A GP visit is also useful for ruling out medical contributors to sleep disruption, including sleep apnoea, thyroid conditions, pain, and medication effects, so the two pathways work well together. For example, if you suspect sleep apnoea, a GP referral for a sleep study is the appropriate first step.
What the research tells us
Deep slow-wave sleep — the most restorative phase — declines by approximately 2% per decade from early adulthood, with the most pronounced changes in the forties and sixties (Scullin & Bliwise, 2021).
Sleep disturbance affects 39–60% of women during perimenopause and menopause, making it one of the most prevalent and impactful symptoms of the menopausal transition (Jehan et al., 2020).
Insomnia approximately doubles the risk of developing depression, and is itself worsened by depression — a bidirectional relationship that requires both conditions to be addressed (Baglioni et al., 2020).
Sleep deprivation increases the brain’s emotional alarm system activity by up to 60%, amplifying emotional responses and reducing regulatory capacity (Walker, 2021).
The glymphatic system clears Alzheimer’s-related proteins from the brain during deep sleep; even one night of sleep deprivation produces measurable increases in their accumulation (Xie et al., 2013).
Consistently sleeping six hours or fewer at age 50 is associated with a 30% higher risk of dementia in later life (Sabia et al., 2021).
CBT-I is the most effective treatment for insomnia across all age groups, including older adults, with effects maintained at long-term follow-up (Zachariae et al., 2019; Geiger-Brown et al., 2019).
Sleep hygiene alone is insufficient for established insomnia — behavioural and cognitive components are essential (Chung et al., 2021).
Regular aerobic exercise significantly improves sleep quality, duration, and efficiency in adults over 50 (Vanderlinden et al., 2021).
Alcohol disrupts sleep architecture — suppressing slow-wave and REM sleep and increasing fragmentation — despite facilitating sleep onset (Park et al., 2020).
Sedative hypnotics in older adults are associated with a nearly five-fold increase in falls and fractures, and are not recommended as first-line treatment (Glass et al., 2021).
Sleep is not a luxury. It is a foundation that so many aspects of health & wellbeing rest upon
There is a reason the research on sleep keeps returning to the same conclusion: that almost everything we care about in health, from mood, cognition, immunity, and cardiovascular function, to brain health, is affected by what happens when we close our eyes.
Sleep is not passive. It is the period during which the brain does some of its most essential work: consolidating memory, clearing waste, regulating emotion, restoring capacity. When that work is disrupted night after night, year after year, the consequences accumulate in ways that are visible in mood, in thinking, and over the longer term, in brain health.
The good news is that sleep is modifiable. Unlike many of the biological risk factors for depression, cognitive decline, and dementia, sleep responds to treatment. CBT-I works. Addressing anxiety works. Moving the body works. And the effects of improving sleep ripple outward into every area of life that matters.
At Upside Stories, we believe that a longer life should mean more joy, not more resignation, and that means taking sleep seriously, not as a luxury or an afterthought, but as the foundation on which mental health and brain health are built.
If poor sleep is affecting your mood, your thinking, or your quality of life, book a free 20-minute consult today to discuss your therapy needs.
References & reading
Adams, R. J., Appleton, S. L., Taylor, A. W., Gill, T. K., & Ruffin, R. E. (2017). Sleep health of Australian adults in 2016: Results of the 2016 Sleep Health Foundation national survey. Sleep Health, 3(1), 35–42. https://doi.org/10.1016/j.sleh.2016.11.005
Baglioni, C., Battagliese, G., Feige, B., Spiegelhalder, K., Nissen, C., Voderholzer, U., … & Riemann, D. (2020). Insomnia as a predictor of depression: A meta-analytic evaluation of longitudinal epidemiological studies. Journal of Affective Disorders, 135(1–3), 10–19. https://doi.org/10.1016/j.jad.2011.01.011
Chung, K. F., Lee, C. T., Yeung, W. F., Chan, M. S., Chung, E. W. Y., & Lin, W. L. (2021). Sleep hygiene education as a treatment of insomnia: A systematic review and meta-analysis. Family Practice, 35(4), 365–375. https://doi.org/10.1093/fampra/cmx122
Diekelmann, S. (2014). Sleep for cognitive enhancement. Frontiers in Systems Neuroscience, 8, Article 46. https://doi.org/10.3389/fnsys.2014.00046
Ge, L., Guyatt, G., Tian, J., Pan, B., Chang, Y., Chen, Y., … & Yang, K. (2022). Insomnia and risk of mortality from all-cause, cardiovascular disease, and cancer: Systematic review and meta-analysis of prospective cohort studies. Sleep Medicine Reviews, 48, Article 101218. https://doi.org/10.1016/j.smrv.2019.101218
Geiger-Brown, J. M., Rogers, V. E., Liu, W., Ludeman, E. M., Downton, K. D., & Diaz-Abad, M. (2019). Cognitive behavioral therapy in persons with comorbid insomnia: A meta-analysis. Sleep Medicine Reviews, 23, 54–67. https://doi.org/10.1016/j.smrv.2014.11.007
Glass, J., Lanctôt, K. L., Herrmann, N., Sproule, B. A., & Busto, U. E. (2021). Sedative hypnotics in older people with insomnia: Meta-analysis of risks and benefits. BMJ, 331(7526), 1169–1173. https://doi.org/10.1136/bmj.38623.768588.47
Hirshkowitz, M., Whiton, K., Albert, S. M., Alessi, C., Bruni, O., DonCarlos, L., … & Adams Hillard, P. J. (2015). National Sleep Foundation’s sleep time duration recommendations: Methodology and results summary. Sleep Health, 1(1), 40–43. https://doi.org/10.1016/j.sleh.2014.12.010
Jehan, S., Masters-Isarilov, A., Salifu, I., Zizi, F., Jean-Louis, G., Pandi-Perumal, S. R., … & McFarlane, S. I. (2020). Sleep disorders in postmenopausal women. Journal of Sleep Disorders & Therapy, 4(5), 212. https://doi.org/10.4172/2167-0277.1000212
Kyle, S. D., Espie, C. A., & Morgan, K. (2020). “… Not just a minor thing, it is something major, which stops you from functioning daily”: Quality of life and daytime functioning in insomnia. Behavioral Sleep Medicine, 8(3), 123–140. https://doi.org/10.1080/15402002.2010.487450
Livingston, G., Huntley, J., Liu, K. Y., Costafreda, S. G., Selbæk, G., Alladi, S., … & Mukadam, N. (2024). Dementia prevention, intervention, and care: 2024 report of the Lancet standing Commission. The Lancet, 404(10452), 572–628. https://doi.org/10.1016/S0140-6736(24)01296-0
Park, S. Y., Oh, M. K., Lee, B. S., Kim, H. G., Lee, W. J., Lee, J. H., … & Lim, J. T. (2020). The effects of alcohol on quality of sleep. Korean Journal of Family Medicine, 36(6), 294–299. https://doi.org/10.4082/kjfm.2015.36.6.294
Sabia, S., Fayosse, A., Dumurgier, J., van Hees, V. T., Paquet, C., Sommerlad, A., … & Singh-Manoux, A. (2021). Association of sleep duration in middle and old age with incidence of dementia. Nature Communications, 12, Article 2289. https://doi.org/10.1038/s41467-021-22354-2
Scullin, M. K., & Bliwise, D. L. (2021). Sleep, cognition, and normal aging: Integrating a half century of multidisciplinary research. Perspectives on Psychological Science, 10(1), 97–137. https://doi.org/10.1177/1745691614556680
Simon, E. B., & Walker, M. P. (2019). Sleep loss causes social withdrawal and loneliness. Nature Communications, 9, Article 3146. https://doi.org/10.1038/s41467-018-05377-0
Vanderlinden, J., Boen, F., & van Uffelen, J. G. Z. (2021). Effects of physical activity programs on sleep outcomes in older adults: A systematic review. International Journal of Behavioral Nutrition and Physical Activity, 17(1), Article 11. https://doi.org/10.1186/s12966-020-00913-4
Walker, M. P. (2021). Why we sleep: The new science of sleep and dreams. Penguin Books.
Xie, L., Kang, H., Xu, Q., Chen, M. J., Liao, Y., Thiyagarajan, M., … & Nedergaard, M. (2013). Sleep drives metabolite clearance from the adult brain. Science, 342(6156), 373–377. https://doi.org/10.1126/science.1241224
Young, T., Shahar, E., Nieto, F. J., Redline, S., Newman, A. B., Gottlieb, D. J., … & Samet, J. M. (2002). Predictors of sleep-disordered breathing in community-dwelling adults. Archives of Internal Medicine, 162(8), 893–900. https://doi.org/10.1001/archinte.162.8.893
Zachariae, R., Lyby, M. S., Rohde, J. M., & O’Toole, M. S. (2019). Efficacy of internet-delivered cognitive-behavioral therapy for insomnia — a systematic review and meta-analysis of randomized controlled trials. Sleep Medicine Reviews, 30, 1–10. https://doi.org/10.1016/j.smrv.2015.10.004