A sleep study published in July 2017 discovered a link between sleep disturbances and biomarkers of Alzheimer’s disease found in the cerebrospinal fluid. The study was published in Neurology, the medical journal of the American Academy of Neurology.
Findings like these are significant in dementia research because Alzheimer’s disease is a difficult diagnosis to demonstrate objectively. Individuals may claim to just be forgetful and become alarmed thinking that Alzheimer’s is likely to develop. Dementia can also have other causes, with the most common being vascular compromise. The same process that causes heart disease, plaque in the arteries, can also develop in arteries that perfuse the brain. The resulting reduced blood flow to the brain causes decreased function of nerve cells. The first symptom of this vascular dementia is usually impaired memory.
Alzheimer’s is different from vascular dementia in that it affects the nerve cells directly.
When is there enough nerve damage to identify the condition as Alzheimer’s disease?
According to current diagnostic criteria, Alzheimer’s disease occurs when symptoms are severe enough to significantly interfere with work, social activities, or relationships. At that stage, currently available medications like donepezil and memantine are used to slow the progression of the disease.
Aside from clinical observation, are there objective measures of nerve damage in the brain?
Currently doctors use two objective assessments to measure nerve damage linked to Alzheimer’s. The first takes into account plaque formation from the presence of a protein called amyloid, which envelops nerve cells and disrupts the synapses that allow neurons to communicate. The other involves a protein called tau, which tangles the fibers that exit nerve cells.
Amyloid levels in cerebrospinal fluid are usually lower in the presence of Alzheimer’s disease. It’s thought that the reduced levels of amyloid in the cerebrospinal fluid indicate that amyloid has deposited in the plaques in the brain. Research has also found that levels of phospho-tau are increased in the cerebrospinal fluid; the level of tau probably reflects the intensity of the neuronal damage and degeneration.
Though different processes may be at play, there is a genetic theory that explains why some people may have an excess of these proteins. Certain people carry a version of the gene apolipoprotein E, or APOE, which suggests a familial predisposition to the disease. Other theories suggest a nutritional basis behind Alzheimer’s, or other elements that may lead to the disease.
Using these objective measures can help to identify individuals at an early stage so attempts to modify some leading factors for development of the disease can be initiated. Alzheimer’s disease currently has no cure.
How does sleep play a part in the development of Alzheimer’s disease?
The association of sleep disturbances and Alzheimer’s disease has been described in medical literature as an association. There are many theories that aim to explain the link.
One theory suggests that failure to initiate and maintain sleep due to degradation of the suprachiasmatic nucleus, which is the clock of the brain, then leads to difficulties with behavior. This causes changes in the wake/sleep schedule, which further destabilizes the ability to get good sleep. The end result is confusion that leads to anger and altered behavior called sundowning.
The significance of the July 2017 sleep study published in Neurology is the discovery of objective measures of the anatomical degeneration of the brain associated with poor sleep. There is evidently great benefit in maintaining healthy sleep if you want to maintain a healthy, intact brain.
It should be noted that this association of abnormal markers was not universal to all types of sleep disorders. There was no strong association when obstructive sleep apnea was the cause of the sleep disturbance, and obstructive sleep apnea did not appear to affect levels of the biomarkers in the cerebrospinal fluid. The study’s authors did offer that it’s still not clear if the disease directly affects quality of sleep, or if sleep directly affects development of the disease.
The take away point is that sustained inadequate sleep hygiene practices may be a stronger risk factor in the development of Alzheimer’s disease because this tends to be more prevalent in the older population. What’s encouraging is that sleep is a potentially modifiable risk factor for Alzheimer’s disease. The treatment in this case would also not be traditional medications for Alzheimer’s disease. Instead, increasing daytime activities and planned exposure to bright light at specific time intervals might be more helpful to reduce daytime sleepiness and therefore help prevent this sleep disorder-associated dementia.
Because many older patients already take medications for a host of other conditions, it’s important to consider that many of these medications have an effect on sleep. Beta-blockers cross the brain barrier and have been known to cause insomnia by interfering with melatonin receptors. Antidepressants can cause vivid dreaming or nightmares by affecting the latency and percentage of rapid eye movement or REM cycles.
A doctor should take a thorough history and do an assessment of all medications and lifestyle habits (including sleep patterns or complaints) so that sleep disorder-associated dementia is considered when assessing early Alzheimer’s disease. Clearly intercepting sleep issues may help to prevent or delay the onset of Alzheimer’s disease.
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Eli Hendel, M.D., is a board-certified internist/pulmonary specialist with board certification in Sleep Medicine. An Assistant Clinical Professor of Medicine at Keck-University of Southern California School of Medicine, and Qualified Medical Examiner for the State of California Department of Industrial Relations, his areas include asthma, COPD, sleep disorders, obstructive sleep apnea, and occupational lung diseases. Favorite hobby? Playing jazz music. Find him on Twitter @Lung_doctor.