Evaluation of distinct and similar pathological features between diabetes and Alzheimer’s disease
DOI:
https://doi.org/10.17179/excli2026-9429Keywords:
Type 2 diabetes, type 1 diabetes, Alzheimer's disease, islet beta-cell, islet alpha-cell, insulin resistanceAbstract
Type 1 diabetes (T1D), type 2 diabetes (T2D) and Alzheimer’s disease (AD), which are heterogeneous multifactorial diseases, have become major global healthcare burdens and significant concerns for the future. Historically, the pathogeneses of these diseases were regarded as being largely distinct, but recent research suggests that this view is now outdated, with a lack of insulin and/or insulin resistance playing an important role in both forms of diabetes and AD. The current state of knowledge on the epidemiology, aetiology, and pathogenesis of T1D, T2D, and AD is summarised in this review. The evidence demonstrating overlapping pathological features between these diseases is also discussed here. Studies have demonstrated that islet autoimmunity, dysfunctional glucagon secretion, insulin resistance and islet amyloidosis manifest in both T1D and T2D. AD has been suggested to be type 3 diabetes (T3D), due to the associated abnormal brain insulin resistance, which is speculated to drive the progressive pathogenesis. Additionally, T1D and T2D are risk factors for AD and vice versa, and most AD patients also have diabetes or glucose intolerance, indicating bidirectional relationships. Thus, the association between AD and diabetes is already well established. Further understanding the connection between these diseases using recent scientific evidence may allow for the development of more efficient therapeutic strategies, which is highly desirable, given the prevalence of post-diagnosis complications. Evidence suggests that GLP-1R agonists can alleviate the phenotypes of all of these diseases, and these agonists could be used in the future to simultaneously treat them in subjects or prevent/delay their manifestation in at-risk individuals.
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Copyright (c) 2026 Joshua Reed, Stephen C. Bain, Venkateswarlu Kanamarlapudi
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