Beta Amyloid Peptide: Research Paper : Unsaturated mannuronate oligosaccharide ameliorates β-amyloid pathology through autophagy in Alzheimer's disease cell models

Unsaturated mannuronate oligosaccharide ameliorates β-amyloid pathology through autophagy in Alzheimer's disease cell models

Abstract

Unsaturated mannuronate oligosaccharide (MOS) is an enzymatic depolymerization product from alginate-derived polymannuronate (PM). In this study, we investigated for the first time the potential therapeutic effect of MOS on Alzheimer's disease (AD) and its molecular mechanism in N2a-sw cells and 3×Tg-AD primary cortex neurons. Our results showed that MOS ranges from mannuronate dimer to mannuronate undecamer (M2-M11) with an unsaturated nonreducing terminal structure and with a double bond and 1,4-glycosidic linkages. It significantly inhibited the aggregation of amyloid-β (Aβ)1-42 oligomer, decreased expression of Aβ1-42 and reduced levels of amyloid precursor protein (APP) and BACE1. It promoted the autophagy, which involves the inactivation of mTOR signaling pathway and the facilitation of the fusion of autophagosomes and lysosomes. Finally, autophagy inhibitors blocked MOS' anti-AD actions, confirming the involvement of autophagy. In conclusion, MOS from seaweed alginate might be a promising nutraceutical or natural medicine for AD therapy.

Keywords: Alginate; Alzheimer's disease; Amyloid-β; Autophagy; Unsaturated mannuronate oligosaccharide.

This article originally appeared in the "https://pubmed.ncbi.nlm.nih.gov/33142656/" and has their copyrights. We do not claim copyright on the content. This information is for research purposes only. This Blog is made available by publishers for educational purposes only as well as to give you general information and a general understanding , not to provide specific advice. By using this blog site you understand that there is no client relationship between you and the Blog publisher. The Blog should not be used as a substitute for competent research advice.