Alzheimer's disease, a metabolic disorder: Clinical advances and basic model studies (Review)

Abstract

Alzheimer's disease (AD) is a type of neurodegenerative disease characterized by cognitive impairment that is aggravated with age. The pathological manifestations include extracellular amyloid deposition, intracellular neurofibrillary tangles and loss of neurons. As the world population ages, the incidence of AD continues to increase, not only posing a significant threat to the well-being and health of individuals but also bringing a heavy burden to the social economy. There is epidemiological evidence suggesting a link between AD and metabolic diseases, which share pathological similarities. This potential link would deserve further consideration; however, the pathogenesis and therapeutic efficacy of AD remain to be further explored. The complex pathogenesis and pathological changes of AD pose a great challenge to the choice of experimental animal models. To understand the role of metabolic diseases in the development of AD and the potential use of drugs for metabolic diseases, the present article reviews the research progress of the comorbidity of AD with diabetes, obesity and hypercholesterolemia, and summarizes the different roles of animal models in the study of AD to provide references for researchers.

Comprehensive Overview of Alzheimer’s Disease: Etiological Insights and Degradation Strategies

“…Furthermore, sodium-glucose co-transporter-2 inhibitors (SGLT2), such as dapagliflozin and Canagliflozin, restore the mTOR pathway via nutrient-sensitive mechanism, resulting in activated glucose uptake and reduced blood glucose levels, potentially mitigating excitotoxicity in the neurons. This could lead to a reduction in tau phosphorylation and the accumulation of Aβ in AD models [120,121]. Additionally, caspases, Nrf2, and NF-κB indirectly influence this pathway.…”