<i>Monascus purpureus</i> Fermented Product Ameliorates Learning and Memory Impairment in the Amyloid Precursor Protein Transgenic J20 Mouse Model of Alzheimer’s Disease

Abstract

Evidence suggests that various hallmarks such as amyloid overproduction, tau dysfunction, insulin resistance/diabetic mechanisms, and neuroinflammation are associated with Alzheimer’s disease (AD). This study investigated the bioactive functions of ankaflavin (AK) and monascin (MS) in the fermented product of Monascus purpureus and found their abilities to ameliorate AD by modifying several important pathogenic factors including improved cognitive function, reversed behavioral deficits, reduced hippocampal β-amyloid peptide (Aβ) burden, decreased tau hyper-phosphorylation, and reduced neuroinflammation in the J20 mouse model of AD compared to wild type. Monascus purpureus fermented product (MPFP) was suggested to act as a peroxisome proliferator-activated receptor (PPAR)-γ agonist and it was compared against the action of a well-known anti-diabetic PPAR-γ agonist rosiglitazone. MPFP could be a promising therapeutic strategy for disease modification in AD.

Keywords

• Alzheimer’s disease
• transgenic J20 mice
• <i>Monascus purpureus</i> fermented product
• monascin
• ankaflavin
• peroxisome proliferator-activated receptor-γ