ANALYSIS OF THE ASSOCIATION BETWEEN TYPE 2 DIABETES MELLITUS AND THE DEVELOPMENT OF ALZHEIMER'S AND DEMENTIA: COMPLICATIONS AND PREVENTION STRATEGIES

Abstract

Introduction: Alzheimer's disease (AD) is the main cause of dementia in the elderly population, accounting for 60% to 70% of cases, as a consequence it leads to cognitive decline. At the same time, the prevalence of type 2 diabetes mellitus (T2DM) has been increasing, with the metabolic disorder increasing the risk of dementia. The relationship between AD and DM2 is complex and involves risk factors associated with lifestyle and eating habits, as well as the brain-gut axis. Inflammation mediated by cytokines, such as IL-6 and TNF-α, results in exacerbation of AD and contributing to insulin resistance, forming a link between the two conditions. Objective: To analyze and associate AD and Dementia as a complication of DM2, as well as its prevention. Methodology: This is an integrative literature review using the prism method, where articles from the last 5 years were analyzed and selected from the electronic databases: Pubmed and VHL (Virtual Health Library). The following descriptors were used: "Diabetes Mellitus", "Alzheimer's", "Dementia" combined with the Boolean operator "AND". A total of 99 articles were obtained, of which only 12 addressed the objective of the study. Results and Discussion: Studies have shown that T2DM increases the risk of neurodegenerative diseases, such as AD, due to insulin resistance and chronic inflammation. Interventions, such as physical exercise and medications (exenatide and metformin) can help preserve the cognitive function of diabetics. Hypoglycemia and obesity also negatively affect brain health, leading to changes in perfusion and neuronal density. The research seeks to better understand these relationships in order to develop prevention and treatment strategies. Conclusion: The research addresses the effects of systemic inflammation and metabolic alterations by offering new perspectives for interventions aimed not only at controlling T2DM, but also at preserving cognitive function in the at-risk population.