Yeast β-glucan alleviates cognitive deficit by regulating gut microbiota and metabolites in Aβ1-42-induced AD-like mice

Int J Biol Macromol. 2020 Oct 15:161:258-270. doi: 10.1016/j.ijbiomac.2020.05.180. Epub 2020 Jun 6.

Abstract

Alzheimer's disease (AD) is a neurodegenerative disease that remarkably imposes a huge global public health burden. Yeast β-glucans have been incorporated in functional foods and used in prophylactic applications owing to their biological effects. However, few studies had investigated the effects of yeast β-glucans on neurodegenerative diseases. Here, gut microbiota and metabolites SCFAs were analyzed through high-throughput 16S rRNA gene sequencing and GC-MS, respectively. Results indicated that yeast β-glucans could prominently shape the intestinal flora and produce SCFAs. Aβ1-42-induced AD mice treated with small-molecular yeast β-glucan (S-β-Glu) or macro-molecular yeast β-glucan (M-β-Glu) exhibited evident alterations of the composition of the gut microbiota, especially in some beneficial bacteria and inflammatory-related bacteria such as Lactobacillus, Bifidobacterium, Desulfovibrio, Oscillibacter, Mucispirillum, Alistipes, Anaerotruncus, and Rikenella. M-β-Glu regulated gut microbiota act as prebiotics better than S-β-Glu. Correlation analysis demonstrated the key microbiota closely associated with AD-related pathologies and cognition. Moreover, M-β-Glu and S-β-Glu ameliorated neuroinflammation and brain insulin resistance (IR), which played a central role in the process of AD pathology. This study broadened the underlying applications of yeast β-glucans as a novel dietary supplementation to prevent early-stage pathologies associated with AD by regulating gut microbiota and the potential mechanism might be ameliorating brain IR.

Keywords: Alzheimer's disease; Gut microbiota; Insulin resistance; Neuroinflammation; Prebiotics; Yeast β-glucans.

MeSH terms

  • Alzheimer Disease / etiology
  • Alzheimer Disease / metabolism
  • Alzheimer Disease / pathology
  • Amyloid beta-Peptides / adverse effects*
  • Animals
  • Biomarkers
  • Cognition / drug effects*
  • Disease Models, Animal
  • Fungal Polysaccharides / chemistry*
  • Fungal Polysaccharides / pharmacology
  • Gastrointestinal Microbiome / drug effects*
  • Hippocampus / metabolism
  • Insulin / metabolism
  • Male
  • Metagenome
  • Metagenomics
  • Mice
  • Peptide Fragments / adverse effects*
  • Prebiotics
  • RNA, Ribosomal, 16S
  • beta-Glucans / chemistry*
  • beta-Glucans / pharmacology

Substances

  • Amyloid beta-Peptides
  • Biomarkers
  • Fungal Polysaccharides
  • Insulin
  • Peptide Fragments
  • Prebiotics
  • RNA, Ribosomal, 16S
  • amyloid beta-protein (1-42)
  • beta-Glucans