A newly published study in JAMA Network Open has cast fresh light on a potentially serious consequence of obstructive sleep apnoea (OSA): the risk of cerebral microbleeds.

The research, which followed more than 1,400 adults over eight years, suggests that moderate to severe OSA could double the odds of developing these tiny brain bleeds. For anyone concerned about brain health, the findings are an important wake-up call.

Obstructive sleep apnoea is not just about snoring or restless nights. This common disorder, affecting an estimated 935 million adults globally, is defined by repeated bouts of upper airway collapse during sleep.

Each episode often causes the sleeper to awaken briefly or experience drops in blood oxygen levels. While many people are aware of OSA’s impact on sleep quality and daytime alertness, fewer understand its broader effects on the body—especially the brain.

Researchers behind this study wanted to go beyond the obvious. Using a subcohort from the Korean Genome and Epidemiology Study, they selected adults who had completed both polysomnography (a diagnostic test for sleep disorders) and MRI scans at three different points over eight years.

Participants were categorised according to the severity of their OSA: none, mild, or moderate to severe. Importantly, anyone with a prior history of cerebrovascular or cardiovascular disease, or with baseline microbleeds, was excluded. This allowed for a clearer picture of new cases.

The final group included 1,441 individuals with an average age just under 58 at the outset. At baseline, 436 had mild OSA and 193 had moderate to severe OSA. The moderate to severe group featured more men, smokers, drinkers, and higher body mass indices—factors that often cluster with worse sleep apnoea.

What did the results show? At the eight-year follow-up, 7.25% of participants in the moderate to severe OSA group had developed cerebral microbleeds.

In contrast, only 3.33% of those without OSA showed these changes. Even after adjusting for factors such as blood pressure, BMI, exercise habits and genetic predispositions (specifically the APOE-ε4 gene linked to Alzheimer’s disease), moderate to severe OSA remained associated with a twofold increased risk at the final follow-up.

The findings matter because cerebral microbleeds are more than just radiological curiosities. These tiny accumulations of blood products in the brain are closely linked to heightened risk for stroke and dementia. As society ages and the prevalence of both OSA and dementia rises, understanding such risks has never been more relevant.

Why might OSA lead to microbleeds? Experts point to several plausible explanations. Severe OSA exposes the brain to repeated episodes of low oxygen (hypoxia), oxidative stress, and inflammation during sleep. These stresses may directly impair the lining of small blood vessels—the endothelium—making them more likely to leak or bleed.

The study took pains to control for confounders that could cloud the analysis. Researchers checked if the relationship held even after excluding people who used continuous positive airway pressure (CPAP), a common OSA treatment.

They also looked at genetic risk factors for Alzheimer’s disease by analysing subgroups with APOE-ε4 data available. Results remained consistent: moderate to severe OSA continued to predict higher risk of cerebral microbleeds.

A few caveats are warranted, though. All participants were Korean adults, which limits how easily these results can be extended to other ethnicities or populations. Most were middle-aged or older; studies in younger people might reveal different patterns. The number of participants with severe OSA at baseline was also relatively small—less than 200—so more research is needed in larger groups.

There were other limitations too. Brain imaging was not equally sensitive at all timepoints; more advanced techniques might have detected additional microbleeds. Different scanners were used over time, possibly affecting results. Some health and lifestyle data were self-reported and therefore subject to error or bias. The study also lacked detailed information on how consistently those using CPAP actually adhered to therapy.

Selection bias could not be entirely ruled out either, since participants with missing data were excluded from analysis. The cohort may also have been healthier overall than the general population due to long-term participation requirements—a common issue in longitudinal research.

Despite these limitations, the evidence is strong enough to raise important questions about prevention and management. Addressing OSA early could be crucial not just for better sleep but for preserving long-term brain health. Timely diagnosis and treatment—whether by CPAP machines or other interventions—might help prevent microbleeds and their downstream consequences.

What should people take away from this? The science suggests that moderate to severe OSA is far from harmless. It is not merely a condition that makes you feel tired during the day; it may contribute directly to physical changes in the brain that raise the risk of stroke or dementia years down the line.

Experts urge that preventive measures for OSA—weight management, avoiding alcohol before bed, quitting smoking, and seeing a doctor for persistent snoring or daytime fatigue—could help reduce these risks. Early diagnosis is particularly important. If you suspect you have sleep apnoea, seeking assessment and starting treatment could be an investment in your future cognitive health.

It is worth noting that while this study shows an association between untreated OSA and microbleeds, it did not directly examine whether treating OSA lowers that risk. However, other studies have found benefits from CPAP use in reducing vascular complications associated with OSA. More research is needed specifically on whether effective treatment can reverse or halt microbleed formation.

The study’s strength lies in its long-term follow-up and rigorous adjustment for confounders such as hypertension, diabetes, BMI and genetic factors. This robustness lends weight to the findings even as scientists call for further research—especially involving diverse populations and younger age brackets.

Underlying mechanisms remain a topic for future investigation. Inflammation and oxidative stress appear likely culprits but exactly how and why OSA triggers microbleeds needs more exploration. Unravelling these mechanisms could open doors for new therapies targeting both OSA and its vascular consequences.

For now, what emerges from this research is clear: obstructive sleep apnoea is not just a nighttime nuisance but a potentially serious medical condition with far-reaching impacts on brain health.

Anyone experiencing symptoms should consider talking to a healthcare professional about assessment and possible interventions. The evidence increasingly supports taking sleep—and its disruption—seriously.

As our understanding of brain health evolves, studies like this reinforce the interconnectedness of different body systems. A good night’s sleep is not only about feeling refreshed; it could also be vital insurance against some of life’s most feared neurological illnesses.