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Type 2 diabetes potentially accelerates brain aging
The executive function, processing speed, and gray matter decrease in patients with type 2 diabetes mellitus.
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Type 2 diabetes mellitus (T2DM) is a global burden diagnosed in about 7% of the population. Patients with T2DM are at a greater risk of developing neurological disorders, like Alzheimer’s disease and dementia. Research indicates that T2DM is associated with brain atrophy and cognitive decline.
Despite the established connection, a neurocognitive assessment is not part of routine clinical care for patients affected by T2DM. Since T2DM is usually diagnosed in middle age, it is often difficult to associate the cognitive decline with T2DM. Also, there are insufficient studies examining the neurocognitive changes across the lifespan in patients with T2DM compared to age-matched subjects. This means it is unknown whether the neurological changes are due to T2DM or exacerbation of age-related decline. Additionally, the impact of T2DM treatment on cognitive function remains to be explored.
Clinical protocols for diagnosing T2DM focus on peripheral biomarkers, like blood glucose, insulin, and fat percentage. However, the neurological effects of the disease manifest long before they could be detected by biomarkers. It means that damage sustained from T2DM could reach irreversible stages by the time it is detected. Therefore, there should be a focus on how to prevent them.
Antal et al. examined the UK Biobank neurocognitive lifespan dataset and then compared it to a meta-analysis of 94 studies to address the abovementioned gaps. Secondly, they examine the causes of brain aging (accelerated brain aging due to T2DM or a pathway specific to the disease). Thirdly, the researchers tried to estimate whether chronicity of the condition or treatment play a part in neurocognitive changes.
The UK Biobank dataset included over twenty thousand subjects between 50 and 80 years. Regarding cognitive effects, results revealed that the executive function (group of mental skills, including working memory, thinking, and self-control) decreased more (13.1% beyond age-related decline of 1.9%) in those with T2DM. Also, processing speed decreased by 6.7% in those with T2DM beyond age-related decline of 1.5%. Gray matter decreased in patients with T2DM, where the ventral striatum (implicated in decision making) showed a 6.2% further reduction beyond the 1% age-related decrease. Further analysis revealed that T2DM accelerated neurodegenerative age-related effects by 26%, and treatment with metformin did not impact cognition or brain atrophy.
The authors concluded that T2DM potentially accelerates normal brain aging. They suggested that neuroimaging could be a useful biomarker utilized with other measures that assess T2DM control and medication efficacy. Also, they highlighted the importance of developing a brain-based biomarker for T2DM and therapeutic options that target the resultant neurocognitive decline.
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Type 2 diabetes mellitus (T2DM) is a global burden diagnosed in about 7% of the population. Patients with T2DM are at a greater risk of developing neurological disorders, like Alzheimer’s disease and dementia. Research indicates that T2DM is associated with brain atrophy and cognitive decline.
Despite the established connection, a neurocognitive assessment is not part of routine clinical care for patients affected by T2DM. Since T2DM is usually diagnosed in middle age, it is often difficult to associate the cognitive decline with T2DM. Also, there are insufficient studies examining the neurocognitive changes across the lifespan in patients with T2DM compared to age-matched subjects. This means it is unknown whether the neurological changes are due to T2DM or exacerbation of age-related decline. Additionally, the impact of T2DM treatment on cognitive function remains to be explored.
Clinical protocols for diagnosing T2DM focus on peripheral biomarkers, like blood glucose, insulin, and fat percentage. However, the neurological effects of the disease manifest long before they could be detected by biomarkers. It means that damage sustained from T2DM could reach irreversible stages by the time it is detected. Therefore, there should be a focus on how to prevent them.
Antal et al. examined the UK Biobank neurocognitive lifespan dataset and then compared it to a meta-analysis of 94 studies to address the abovementioned gaps. Secondly, they examine the causes of brain aging (accelerated brain aging due to T2DM or a pathway specific to the disease). Thirdly, the researchers tried to estimate whether chronicity of the condition or treatment play a part in neurocognitive changes.
The UK Biobank dataset included over twenty thousand subjects between 50 and 80 years. Regarding cognitive effects, results revealed that the executive function (group of mental skills, including working memory, thinking, and self-control) decreased more (13.1% beyond age-related decline of 1.9%) in those with T2DM. Also, processing speed decreased by 6.7% in those with T2DM beyond age-related decline of 1.5%. Gray matter decreased in patients with T2DM, where the ventral striatum (implicated in decision making) showed a 6.2% further reduction beyond the 1% age-related decrease. Further analysis revealed that T2DM accelerated neurodegenerative age-related effects by 26%, and treatment with metformin did not impact cognition or brain atrophy.
The authors concluded that T2DM potentially accelerates normal brain aging. They suggested that neuroimaging could be a useful biomarker utilized with other measures that assess T2DM control and medication efficacy. Also, they highlighted the importance of developing a brain-based biomarker for T2DM and therapeutic options that target the resultant neurocognitive decline.
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Dr. Ana Baroni MD. Ph.D.
Scientific & Medical Advisor
Quality Garant
Ana has over 20 years of consultancy experience in longevity, regenerative and precision medicine. She has a multifaceted understanding of genomics, molecular biology, clinical biochemistry, nutrition, aging markers, hormones and physical training. This background allows her to bridge the gap between longevity basic sciences and evidence-based real interventions, putting them into the clinic, to enhance the healthy aging of people. She is co-founder of Origen.life, and Longevityzone. Board member at Breath of Health, BioOx and American Board of Clinical Nutrition. She is Director of International Medical Education of the American College of Integrative Medicine, Professor in IL3 Master of Longevity at Barcelona University and Professor of Nutrigenomics in Nutrition Grade in UNIR University.
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