Sleep apnoea may cause early cognitive decline

Patients with obstructive sleep apnoea often show cognitive deficits, but these have traditionally been attributed to comorbidities such as systemic hypertension, cardiovascular and metabolic diseases, and type 2 diabetes. Now, researchers have shown for the first time that OSA itself is sufficient to cause early cognitive decline.

Obstructive sleep apnoea (OSA) is a potentially dangerous condition — during sleep, the throat muscles of people with OSA relax and block the airflow into the lungs, so that they repeatedly stop breathing. Common symptoms of OSA include restless sleep, loud snoring, daytime sleepiness and prolonged headaches in the morning.

Major risk factors for OSA include middle or old age, being obese, smoking, chronic nasal blockage, high blood pressure and being male. Now, researchers from the UK, Germany and Australia have shown that in middle-aged men, OSA can cause early cognitive decline, even in patients who are otherwise healthy. Their results have been published in Frontiers in Sleep.

“We show poorer executive functioning and visuospatial memory and deficits in vigilance, sustained attention, and psychomotor and impulse control in men with OSA. Most of these deficits had previously been ascribed to comorbidities,” said Dr Ivana Rosenzweig, head of the Sleep and Brain Plasticity Centre at King’s College London and lead author of the study.

“We also demonstrated for the first time that OSA can cause significant deficits in social cognition.”

Rare cohort without comorbidities

Rosenzweig and colleagues studied a group of 27 men between the ages of 35 and 70 with a new diagnosis of mild to severe OSA but without any comorbidities. Such patients are relatively rare, because most men and women with OSA have comorbidities such as cardiovascular and metabolic disease, stroke, diabetes, chronic systemic inflammation or depression.

The men were not currently smokers or alcohol abusers, and were not obese according to their body mass index (BMI). As a control, the researchers studied a group of seven age-, BMI-, and education-matched men without OSA. The OSA diagnosis was confirmed by a so-called WatchPAT test of their respiratory function during sleep at home, and also by video-polysomnography at the King’s College sleep centre. The scientists also tested the subjects’ cognitive function with the Cambridge Neuropsychological Test Automated Battery (CANTAB) of tests.

Premature cognitive decline

The results showed that patients with severe OSA had poorer vigilance, executive functioning, short-term visual recognition memory, and social and emotion recognition than the matched controls. Patients with mild OSA performed better in these domains than patients with severe OSA, but worse than the controls.

“The most significant deficits … were demonstrated in the tests that assess both simultaneous visual matching ability and short-term visual recognition memory for non-verbalisable patterns, tests of executive functioning and cued attentional set shifting, in vigilance and psychomotor functioning, and lastly, in social cognition and emotion recognition,” the authors wrote.

The authors conclude that OSA is sufficient to cause these cognitive deficits, which previous studies had attributed to the most common comorbidities of OSA such as systemic hypertension, cardiovascular and metabolic diseases, and type 2 diabetes.

Unclear mechanism

So what is the mechanism by which OSA causes premature cognitive decline? The authors speculated that the cognitive deficits are due to intermittent low oxygen and high carbon dioxide in the blood, changes in blood flow to the brain, sleep fragmentation and neuroinflammation in OSA patients.

“This complex interplay is still poorly understood, but it’s likely that these lead to widespread neuroanatomical and structural changes in the brain and associated functional cognitive and emotional deficits,” Rosenzweig said.

Whether comorbidities have similar negative effects on cognition above and beyond those caused directly by OSA is not yet clear. “However,” Rosenzweig said, “our findings suggest that comorbidities likely worsen and perpetuate any cognitive deficits caused directly by OSA itself.

“What remains to be clarified in future studies is whether comorbidities have an additive or synergistic effect on the latter deficits, and whether there is a difference in brain circuitry in OSA patients with or without comorbidities.”

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