In the elderly without dementia, excessive sleepiness during the day would be associated with increased accumulation of the amyloid cerebral protein, a marker of Alzheimer’s disease. In treating people with excessive daytime sleepiness, it may be possible to prevent the potential development of dementia.
American researchers at the Mayo Clinic have found the association between excessive daytime sleepiness (the “fat” nap) and the accumulation of amyloid β protein in the brain, a biomarker of Alzheimer’s disease.
By identifying early people with excessive daytime sleepiness, it may be possible to provide timely treatment, reduce the progression of cerebral amyloidosis and prevent the possible development of dementia.
Aging and drowsiness
Aging is usually associated with excessive daytime sleepiness, which is itself related to cognitive decline in the elderly. This type of drowsiness is defined as a difficulty in maintaining the desired wakefulness or as a complaint of excessive sleep.
Several studies have already shown an association between excessive daytime sleepiness and an increased risk of dementia, and more specifically the association between excessive daytime sleepiness and pronounced cortical thinning in age-sensitive areas, suggesting accelerated aging of the brain.
Excessive diurnal sleepiness and Alzheimer’s disease
In practice, the accumulation of amyloid β protein occurs quite early in the preclinical stages of Alzheimer’s disease. However, sleep can promote its elimination and, conversely, a disturbed sleep can contribute to its accumulation while participating in the increase of the cerebral synaptic activity contributing to the accumulation of β amyloid protein.
This vicious circle can be stopped according to US researchers. The latter found in an observational study conducted between 2009 and 2016 in 283 people over 70 years of age and not suffering from dementia, that excessive daytime sleepiness was associated with increased accumulation of amyloid β protein in sensitive areas of the brain: the cingulate gyrus and the precuneus.
Based on these observations, people with excessive daytime sleepiness are more vulnerable to brain changes occurring in Alzheimer’s disease.
The researchers plan to focus on new work to determine whether excessive daytime sleepiness is a clinical marker of increased sleep instability, synaptic overload, or the neurodegeneration of wakefulness-promoting centers. Early identification of people with excessive daytime sleepiness could treat their underlying sleep disorders and prevent the development of cerebral amyloidosis.
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