What your eyes reveal about your brain: Diabetic retinopathy and dementia risk
Eye health strongly reflects brain health. A recent South Korean study shows patients with diabetic retinopathy face a notably higher risk of developing dementia. These findings highlight the need for regular eye exams—not just for vision, but also for early detection of broader health concerns.
Ankita Jaykumar is an assistant professor, pharmaceutical sciences at UNT Health Fort Worth and an affiliate faculty at NTERI. Her research focuses on the metabolic alterations in the brain associated with the pathogenesis of cognitive dysfunction. She gives us some insight into this study and the connection between diabetic retinopathy and dementia.
The recent nationwide Korean cohort study found that patients with diabetic retinopathy had a significantly increased risk of developing dementia over roughly 11 years, even after adjusting for multiple risk factors. What do you see as the most compelling biological or clinical mechanisms that could explain this strong association?
Diabetic retinopathy isn't just an eye problem. It mirrors insulin resistance in the brain, making it a valuable biomarker for cognitive health. To put it simply, the underlying factor is insulin resistance. Work from several groups, including ours, suggests that insulin resistance in the Central Nervous System is associated with dementia. Therefore, understanding the mechanisms involving insulin resistance in the retina and the brain is critical to understanding and dissecting the molecular mechanisms involved.
The study showed that both moderate and severe diabetic retinopathy were linked to elevated dementia risk. How should clinicians interpret diabetic retinopathy severity in the context of dementia risk stratification?
Clinicians should interpret diabetic retinopathy severity as a strong indicator for dementia risk, meaning moderate to severe diabetic retinopathy signals significantly higher risk, prompting proactive cognitive screening and management, as diabetic retinopathy acts as a key biomarker beyond diabetes itself. Both the presence and increasing severity of diabetic retinopathy increase dementia risk, highlighting the need for aggressive diabetes control and early dementia detection.
The analysis reported increased risk for both Alzheimer’s disease and vascular dementia among those with diabetic retinopathy. How might diabetic retinopathy specifically connect to these two differing dementia subtypes from a pathopsychological standpoint?
There are at least two underlying phenomena in diabetic retinopathy that we need to understand. First is underlying insulin resistance, and the second is microvascular damage in the brain. Diabetic retinopathy is not just an eye problem. It mirrors insulin resistance and microvascular damage in the eye, making it a valuable biomarker both for Alzheimer’s disease and vascular dementia.
The recent review emphasizes the role of vascular dysfunction, such as reduced cerebral blood flow and blood-brain barrier breakdown, initiating cognitive decline. How do you see retinal microvascular changes in diabetic retinopathy reflecting or paralleling these cerebral vascular processes?
The answer to this question lies in the fact that insulin in the brain has been suggested to act as a central regulator of neurovascular coupling. Neurovascular coupling is a key phenomenon that supports brain activity in response to functional demands via coupling brain glucose metabolism with blood flow. This is critical to supporting cognition. In other words, insulin promotes a higher cerebral blood flow, which allows higher glucose metabolism in response to increased functional demands of the brain, such as during learning and memory. In the context of insulin resistance, this fine coupling between glucose metabolism and cerebral blood flow in response to enhanced demands of the brain is lost. Compensatory mechanisms kick in, leading to blood-brain barrier breakdown. Insulin resistance in the retina mirrors the brain, and it is central to cerebral and retinal vascular dysfunction seen in cognitive decline.
Both the retina and brain rely on tightly regulated neurovascular units. In your view, what are the key shared cellular or molecular mechanisms between diabetic retinal microvascular damage and cerebrovascular changes implicated in dementia?
The key shared molecular mechanism is insulin resistance, leading to retinal and cerebral vascular dysfunction implicated in dementia.
Vascular aging and diabetes both promote endothelial dysfunction, arterial stiffness, and impaired perfusion – factors linked to dementia risk. How can clinicians integrate this understanding into prevention strategies that target both ocular and cerebral vascular health?
Clinicians should treat ocular health status as a biomarker for dementia risk. Proactive screening, aggressive diabetes management, and support for healthy lifestyles are essential for prevention and early intervention.
How should ophthalmologists and primary care providers collaborate in monitoring patients with diabetic retinopathy regarding long-term cognitive health?
One of the areas where our health care system could greatly improve is the collaboration between various health specialties and the emphasis on preventing diseases by promoting healthy lifestyle choices. We really need to focus on preventing diseases such as diabetes and addressing the underlying insulin resistance at early stages. This is only possible when there is a conscious shift in how the health care system functions. I do see a ray of hope with these epidemiological studies emphasizing a need for collaboration between different medical specialties and a need for focusing on disease prevention in the early stages of disease pathogenesis.
Could retinal vascular changes serve as an accessible biomarker for early detection of individuals at a heightened risk of cognitive decline? What research or clinical validation might be needed?
Yes, retinal vascular damage could serve as a critical biomarker for early detection of individuals at high risk for cognitive decline. This is based on several epidemiological studies that show a significant association between the two. Factors that influence this association are genetics, such as APOE4 carrier status in patients, which is very highly associated with dementia risk. Other factors are lifestyle choices, underlying diabetes management. These factors are very difficult to control in epidemiological studies, but clinicians can definitely tailor their care to individual patients with several risk factors for cognitive decline.
What gaps remain in understanding how diabetic retinopathy relates to vascular contributions to dementia, and what research directions should our organization prioritize?
The underlying molecular mechanisms involved in how insulin resistance promotes vascular dementia are lacking. There is a need for more collaborative efforts between the visual sciences and neuroscience disciplines to further address these gaps in our understanding.
How might we effectively communicate with patients with diabetes about the importance of both ocular and vascular health in preserving cognitive function?
Newsroom articles such as this are valuable in promoting the awareness that these phenomena are linked. Clinicians also need to advise patients on the impact of diabetes on their cognitive health. I think as the awareness on this matter increases, patients will also proactively consult with their physicians to control diabetes and address the underlying insulin resistance by promoting healthy lifestyle choices to prevent dementia and other detrimental effects on their health in general.
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