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The mechanisms in obesity that cause mild cognitive impairment are similar to those of type 2 diabetes. Fat is a powerful cerebral toxin and risk factor: it causes delayed reaction times in both executive function and attention.
The Vall d’Hebron University Hospital Obesity Unit, part of the Endocrinology and Nutrition Unit, has conducted a study showing the relation between morbid obesity and mild cognitive impairment in young patients. “We know that fat is a powerful cerebral toxin and that obesity is a risk factor for mild cognitive impairment”, explains Dr Andreea Cuidin, head of the Vall d’Hebron University Hospital Obesity Unit and principal investigator of the Vall d’Hebron Research Diabetes and Metabolism Group, headed by Dr Rafael Simó. The study involved 80 patients with morbid obesity in the bariatric surgery programme who were matched by age and sex with 30 healthy controls. All the patients underwent cognitive assessment, a habitual screening test and the Montreal Cognitive Assessment Test (MoCA). In addition, a new test was used, retinal microperimetry, whose usefulness in analysing and monitoring cognitive capacity in patients with type 2 diabetes under 65 years of age has been shown by Vall d’Hebron.
This test is quick and simple and does not depend on the patient’s mood, unlike neurocognitive tests. “It is a physical test in which the patient has to press buttons depending on the lights they see on a screen”, explains Dr Andreea Ciudin.
Retinal microperimetry is a test to diagnose and monitor cognitive disorders in patients with type 2 diabetes. In this regard, Dr Rafael Simó, head of the Endocrinology and Nutrition Department and the Vall d’Hebron Research Diabetes and Metabolism Group, is coordinating the European project RECOGNISED, whose main objective is to explore microperimetry retina assessment as a tool for identifying type 2 diabetes, an independent risk factor for developing cognitive impairment and dementia.
Dr Andreea Ciudin explains that the mechanisms whereby obesity induces cognitive impairment are similar to those in patients with type 2 diabetes. Both diseases involve insulin resistance, which is related to functional alterations (increased white matter permeability, present in early phases, especially in children) and structural alterations (glial activation and neurodegeneration in more advanced stages).
Microperimetry assesses two independent parameters: retinal sensitivity, which is related to neurodegeneration, and visual fixation, which is dependent on complex circuits in the white matter of the brain. Young patients with obesity have an alteration in gaze fixation, correlated to insulin resistance, but not in retina sensitivity, unlike patients with type 2 diabetes, who develop alterations in both parameters. The researchers note that changes to white matter, rather than neurodegeneration, play a fundamental role in fixation alteration as the main nexus between obesity and cognitive impairment.
The patients who took part in the study underwent two tests, the MoCA test and retinal microperimetry, prior to and 12 months after undergoing bariatric surgery for weight loss. A year after the operation, weight loss was significant, the overall memory loss score had improved (due to delayed recall), although deterioration to attention, visual-spatial executive function and microperimetry visual fixation were still detected. This suggests that several areas of the brain might respond differently to bariatric surgery-induced changes during the first year.
This pilot study opens the way to new studies to explore the relation between obesity and cognitive impairment more closely, in order to understand the impact of several weight-loss strategies (diet, drugs, bariatric surgery) and offer the patient personalised care and the best therapeutic option.
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