Vascular Impairment in Alzheimer’s Disease: The Role of Obstructive Sleep Apnea


Sleep apnea is a condition in which a person has one or more pauses in breathing, or very shallow breaths, while they sleep. Then, normal breathing starts again, sometimes with a loud snort or choking sound. When a person’s breath becomes too shallow or actually pauses, their body moves from deep sleep and into light sleep, and this reduces the quality of sleep attained and leads to excessive daytime sleepiness.1 Previous research suggested a link between obstructive sleep apnea syndrome (OSAS) and Alzheimer’s disease. However, how sleep disturbance can affect cognitive impairment is not clear.


This study was conducted to determine whether patients with Alzheimer’s disease and obstructive sleep apnea have vascular, structural, and functional damage at the level of cerebral arteries.2 The study found that the extent of cerebrovascular impairment (impairment of blood flood to the brain) was correlated with the severity of obstructive sleep apnea. Tightening of the carotid arteries (which supply blood to the brain) as assessed by intima-media thickness was also significantly associated with the presence of obstructive sleep apnea. The researchers concluded that their findings demonstrate a correlation between the severity of oxygen desaturation during night time sleep and the impairment of functional and anatomic characteristics of cerebral vessels.


The study population was selected from 211 patients who were referred to a dementia outpatient service by general practitioners due to progressive cognitive impairment. Criteria were used to determine probable Alzheimer’s disease diagnosis and mild to moderate cognitive impairment. Patients with a history of cerebrovascular disease were excluded. Ultimately, the research team evaluated 69 patients without OSAS and 93 patients with OSAS. The patients each participated in an ultrasonographic assessment of common carotid arteries intima-media thickness and carotid plaque index. Cerebrovascular (brain and blood vessels) reactivity to carbon dioxide retention in the middle cerebral arteries was calculated with the Breath-Holding Index. An overnight sleep study was conducted and the researchers recorded the patients’ brain waves (electroencephalography), the oxygen level in their blood (finger pulse oximetry), heart rate (electrocardiography) and breathing (airflow), as well as eye movement (electrooculography), snoring and body position.

The researchers defined sleep apnea as a complete interruption of airflow for a minimum of 10 seconds. They defined hypopnea as a greater than 30% decrease in the amplitude (measure of change over a single period) of airflow for 10 seconds or longer followed by 3% oxygen desaturation and/or arousal. The researchers determined an Apnea/Hypopnea value by dividing the total number of apneas and hypopneas by the total hours of sleep time. Patients were diagnosed as having OSAS if the Apnea/Hypoapnea value was ≥ 5. Patients with an Apnea/Hypoapnea value between 5 and 14 were considered to have mild OSAS. Patients with an Apnea/Hypoapnea value between 15 and 30 were considered to have moderate OSAS. Patients with an Apnea/Hypoapnea value greater than 30 had severe OSAS.


  1. National Heart, Lung and Blood Institute. What is Sleep Apnea? Accessed September 6, 2016.
  2. Buratti L, Viticchi G, Falsetti L, et al. Vascular impairment in Alzheimer’s disease: the role of obstructive sleep apnea. Journal of Alzheimers Disease. 2014;38(2):445-53. doi: 10.3233/JAD-131046.



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