Selenium-enriched foods and their ingredients: As intervention for the vicious cycle between autophagy and overloaded stress responses in Alzheimer's disease

Dysfunctional autophagy induced by excessive reactive oxygen species (ROS) load and inflammation accelerates the development of Alzheimer's disease (AD). Recently, there has been an increasing interest in selenium-enriched ingredients (SEIs), such as selenoproteins, selenoamino acids and selenosugars, which could improve AD through antioxidant and anti-inflammation, as well as autophagy modulating effects. This review indicates that SEIs eliminate excessive ROS by activating the nuclear translocation of nuclear factor erythroid2-related factor 2 (Nrf2) and alleviate inflammation by inhibiting the mitogen-activated protein kinases (MAPKs)/nuclear factor kappa-B (NF-kappa B) pathway. Furthermore, they can activate the adenosine 5'-monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) pathway, and subsequently promote amyloid beta (A beta) clearance and reduce memory impairments. SEIs are ubiquitous in many plants and microorganisms, such as Brassicaceae vegetables, yeast, and mushroom. Enzymatic hydrolysis, as well as physical processing, such as thermal, high pressure and microwave treatment, are the main techniques to modify the properties of dietary selenium. This work highlights the fact that SEIs can inhibit inflammation and oxidative stress and provides evidence that supports the potential use of these dietary materials to be a novel strategy for improving AD.

Automated summary

Excessive ROS and inflammation lead to dysfunctional autophagy in Alzheimer's disease. Selenium-enriched ingredients (SEIs), including selenoproteins, selenoamino acids, and selenosugars, have shown potential in improving AD through antioxidant, anti-inflammatory, and autophagy-modulating effects. This review highlights that SEIs can eliminate ROS, alleviate inflammation, activate the AMPK/mTOR pathway, promote Aβ clearance, and reduce memory impairments, making them a potential novel strategy for AD treatment.