OSA May Trigger Earlier Cognitive Decline in Men
A new small study suggests that obstructive sleep apnea (OSA) could cause cognitive decline at an earlier age in men.
“We show poorer executive functioning and visuospatial memory and deficits in vigilance, sustained attention, and psychomotor and impulse control in men with OSA,” said neuropsychiatrist Ivana Rosenzweig from King’s College London. UK.
“Most of these deficits had previously been ascribed to comorbidities,” she added. “We also demonstrated for the first time that OSA can cause significant deficits in social cognition.”
The study involved 27 men, of whom 16 (mean age, 43) had a new diagnosis of mild OSA and 11 (mean age, 47) were diagnosed with severe OSA. None had comorbidities, which is “rare,” according to the researchers. Most people with OSA have co-morbidities such as cardiovascular and metabolic disease, stroke, diabetes, chronic systemic inflammation, or depression.
Another 7 men, matched for patient demographics, did not have OSA and were used as a control group.
In cognitive tests using the Cambridge Neuropsychological Test Automated Battery, 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-verbalizable patterns;tests of executive functioning and cued attentional set shifting; in vigilance and psychomotor functioning; and lastly, in social cognition and emotion recognition,” wrote the authors.
“Our findings suggest that distinct, OSA-driven processes may be sufficient for cognitive changes to occur as early as in middle age, in otherwise healthy individuals,” the authors conclude.
The authors speculate 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,” said Rosenzweig.
Whether co-morbidities have similar negative effects on cognition above and beyond those caused directly by OSA is not yet clear.
“Our study is a proof of concept,” said Rosenzweig. “However, our findings suggest that co-morbidities likely worsen and perpetuate any cognitive deficits caused directly by OSA itself.”
“What remains to be clarified in future studies is whether co-morbidities 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 co-morbidities.”