Alzheimer's disease from a diabetic brain: Exploring the molecular process to determine the potential therapy target from marine sources

Abstract

Background: The prevalence of Alzheimer’s Disease (AD) among Type 2 Diabetes Mellitus (T2D) patients has reached almost 30%. Despite the rapid development, treatments for patients with T2D have not succeeded in controlling the neurodegenerative processes that occur in these patients' brains, leading to AD pathology. Several studies have demonstrated that marine sources can inhibit several AD pathogenesis pathways in T2D patients. This review aimed to determine the effect of marine species-sourced compounds at the molecular level in inhibiting and preventing the pathogenesis of AD in T2D patients.    Method: Combinations of several terms were used to search for peer-reviewed literature published in PubMed, Scopus, and Google Scholar.    Result: Marine organisms-sourced compounds inhibited various target signalling pathways between T2D and AD, such as an inhibitor of β-site-amyloid precursor protein cleaving enzyme 1 (BACE1) also known as β-secretase, glycogen synthase kinase-3 beta (GSK3B), insulin degradation enzyme (IDE), the mammalian target of rapamycin (mTOR), nuclear factor kappa-light-chain-enhancer (NF-κb), and nuclear factor erythroid 2-related factor 2 (Nrf2).     Conclusion: Marine sources can be considered as a potential therapy to prevent or slow AD progression in T2D patients.