Medically reviewed by
Dacelin St Martin, MD
Triple board-certified in Sleep Medicine,
Internal Medicine, and Pediatrics.
Sleep & Alzheimer’s The Connection | What the Studies Show | Clinical Importance
Overview
As the average human lifespan increases, the number of people with neurodegenerative diseases tends to increase.
Alzheimer’s disease (AD) is the most common neurodegenerative disease worldwide, accounting for 60 to 80 percent of all dementia cases.[1]
Although some genetic factors are known to be involved in the pathophysiology of Alzheimer’s disease, new findings suggest that some lifestyle factors may also be involved.[2]
One of these factors thought to be related to the formation of Alzheimer’s is sleep disorders.[2] Although the relationship between sleep disorders and Alzheimer’s development has not been definitively clarified, recent research suggests that brain inflammation may play an important role.[3]
Sleep & Alzheimer’s: The Connection
It’s known that sleep is essential for memory consolidation,[4] and sleep disorders are frequently seen in Alzheimer’s patients.
On the other hand, while it was thought that there was a one-way relationship between these two conditions in the past, it is now known that sleep disorders can be not only the result of Alzheimer’s disease but also one of the causes.
Although it’s generally said that all sleep disorders can be associated with dementia, the most apparent sleep disorder in this regard is insomnia.
In a large meta-analysis, sleep duration of fewer than 5 hours or longer than 9 hours was associated with impaired cognitive function in people over 55.[5]
Also, according to a recent meta-analysis, the relative risk of developing Alzheimer’s disease is 1.5 in persons with sleep disturbance.[6] This relative risk is comparable with other modifiable risk factors, such as diabetes mellitus, smoking, physical inactivity, social isolation, and late-life depression.
Inflammation is an indispensable part of the healing process in the body, created by our immune system.
On the other hand, prolonged inflammation in specific tissues is one of the underlying mechanisms of many diseases, such as Alzheimer’s. Neuroinflammation (brain inflammation) is vital in the formation and progression of Alzheimer’s disease.[7]
In the brain inflammation process, microglia, one of the immune system cells, play the leading role. In this process, activated microglia cells, for various reasons, lead to significant changes in the metabolism of amyloid beta and tau protein, which are the most basic hallmarks of Alzheimer’s disease.
What the Studies Show
Recent studies indicate that age-related brain inflammation decreases fast sleep spindles through tau protein metabolism and neuronal synaptic integration, which increases the risk of Alzheimer’s disease through long-term memory retention.[3]
All these findings place sleep disorders in an essential position in the pathophysiology of Alzheimer’s.
In this most recent study, decreased fast sleep spindles with brain inflammation markers were seen in people at risk but not yet diagnosed with Alzheimer’s, suggesting that this sleep marker may be one of the earliest signs of Alzheimer’s in the preclinical stage.[3]
Sleep spindles are specific EEG rhythms that are frequently seen in NREM sleep. These are sudden changes in frequency and amplitude in the EEG signal and usually last for 1-3 seconds.[8]
Sleep spindles are known to protect sleep quality and promote the memory process by inhibiting external sensory stimuli.[9]
Animal studies show that sleep spindles reflect the communication between different brain regions during the learning process.
Another crucial biological issue related to dementia and Alzheimer’s is the circadian rhythm, which can deteriorate with age. In advanced stages of Alzheimer’s disease, it can even be disrupted entirely, causing the person to sleep at random times during the day.[10]
Clinical Importance
The details of the relationship between sleep disorders and Alzheimer’s disease are slowly being clarified, but there is still much to explore.
On the other hand, new findings on brain inflammation linking these two disorders show that sleep analysis can be a potential marker in the diagnosis and follow-up of treatment efficacy of Alzheimer’s disease.
After collecting sufficient scientific evidence, it may be possible to detect and closely monitor patients who have not yet been clinically diagnosed but are at risk for Alzheimer’s disease with a comprehensive sleep analysis.
After the detection of these patients, the treatment of sleep disorders can reduce brain inflammation levels. Thus, avoiding or delaying the onset of Alzheimer’s disease may be possible.
In addition, treatment of sleep disorders can significantly reduce the risk of developing Alzheimer’s, as sleep disorders are also associated with other Alzheimer’s risk factors such as social isolation, physical inactivity, and diabetes mellitus.
References:
- Erkkinen, M. G., Kim, M. O., & Geschwind, M. D. (2018). Clinical Neurology and Epidemiology of the Major Neurodegenerative Diseases. Cold Spring Harbor perspectives in biology, 10(4), a033118. https://doi.org/10.1101/cshperspect.a033118
- Livingston, G., Sommerlad, A., Orgeta, V., Costafreda, S. G., Huntley, J., Ames, D., Ballard, C., Banerjee, S., Burns, A., Cohen-Mansfield, J., Cooper, C., Fox, N., Gitlin, L. N., Howard, R., Kales, H. C., Larson, E. B., Ritchie, K., Rockwood, K., Sampson, E. L., Samus, Q., … Mukadam, N. (2017). Dementia prevention, intervention, and care. Lancet (London, England), 390(10113), 2673–2734. https://doi.org/10.1016/S0140-6736(17)31363-6
- Mander, B. A., Dave, A., Lui, K. K., Sprecher, K. E., Berisha, D., Chappel-Farley, M. G., Chen, I. Y., Riedner, B. A., Heston, M., Suridjan, I., Kollmorgen, G., Zetterberg, H., Blennow, K., Carlsson, C. M., Okonkwo, O. C., Asthana, S., Johnson, S. C., Bendlin, B. B., & Benca, R. M. (2022). Inflammation, tau pathology, and synaptic integrity associated with sleep spindles and memory prior to β-amyloid positivity. Sleep, zsac135. Advance online publication. https://doi.org/10.1093/sleep/zsac135
- Westermann, J., Lange, T., Textor, J., & Born, J. (2015). System consolidation during sleep – a common principle underlying psychological and immunological memory formation. Trends in neurosciences, 38(10), 585–597. https://doi.org/10.1016/j.tins.2015.07.007
- Lo, J. C., Groeger, J. A., Cheng, G. H., Dijk, D. J., & Chee, M. W. (2016). Self-reported sleep duration and cognitive performance in older adults: a systematic review and meta-analysis. Sleep medicine, 17, 87–98. https://doi.org/10.1016/j.sleep.2015.08.021
- Shi, L., Chen, S. J., Ma, M. Y., Bao, Y. P., Han, Y., Wang, Y. M., Shi, J., Vitiello, M. V., & Lu, L. (2018). Sleep disturbances increase the risk of dementia: A systematic review and meta-analysis. Sleep medicine reviews, 40, 4–16. https://doi.org/10.1016/j.smrv.2017.06.010
- Leng, F., & Edison, P. (2021). Neuroinflammation and microglial activation in Alzheimer disease: where do we go from here?. Nature reviews. Neurology, 17(3), 157–172. https://doi.org/10.1038/s41582-020-00435-y
- Weng, Y. Y., Lei, X., & Yu, J. (2020). Sleep spindle abnormalities related to Alzheimer’s disease: a systematic mini-review. Sleep medicine, 75, 37–44. https://doi.org/10.1016/j.sleep.2020.07.044
- Lüthi A. (2014). Sleep Spindles: Where They Come From, What They Do. The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry, 20(3), 243–256. https://doi.org/10.1177/1073858413500854
- Van Erum, J., Van Dam, D., & De Deyn, P. P. (2018). Sleep and Alzheimer’s disease: A pivotal role for the suprachiasmatic nucleus. Sleep medicine reviews, 40, 17–27. https://doi.org/10.1016/j.smrv.2017.07.005
