Currently, Alzheimer’s disease (AD) is a neurodegenerative disease with the largest number of patients and the widest range of impact in the world, and its pathogenic mechanism has not yet been fully understood. Emerging evidence has shown that the gut microbiota can regulate the development and health of the brain via gut-brain axis. Probiotics are a group of live microorganisms that maintain intestinal microecological balance. In recent years, probiotics and their metabolites or probiotic fermented foods have received great attention for their role in alleviating neurodegenerative diseases including AD. Herein, this paper reviews the progress in the past five years in the application of single-strain or multiplestrain probiotics, probiotic fermented foods, and probiotics combined with other drugs for alleviating AD, and expounds the relevant mechanisms and existing problems. We expect this review to provide new ideas for the application of probiotics in the prevention and treatment of AD.

This study aimed to investigate the impact of three postbiotics at different doses on cognitive function in a rat model of Alzheimer’s disease (AD) induced by D-galactose combined with AlCl₃. Specific pathogen-free (SPF) Wistar rats were randomly divided into nine groups: control (Ctrl), AD model, positive drug (donepezil hydrochloride), low-dose (10⁸ CFU/kg) and high-dose (10⁹ CFU/kg) Bifidobacterium animalis spp. lactis IOBL07, Lactiplantibacillus plantarum IOB602 and L. paracasei IOB413. The Ctrl group was intraperitoneally and orally administered with normal saline, while all other experimental groups were subjected to intraperitoneal injection of D-galactose and oral gavage of AlCl₃. The model induction period lasted for 13 consecutive weeks. At 1 h following the last injection and oral gavage, the intervention groups were orally administered with donepezil hydrochloride or postbiotics, whereas the Ctrl and AD groups were given an equivalent volume of normal saline. The Morris water maze was used to assess the learning and memory capacities of the rats in each group. Additionally, the content and immunofluorescence intensity of amyloid β-protein (Aβ) in hippocampal tissues were determined. Histopathological changes in the small intestine were examined along with changes in the intestinal microbiota. The levels of lipopolysaccharide (LPS) in feces, serum, and hippocampal tissues were determined as well as the relative mRNA transcription levels of Toll-like receptor 4 (TLR4), NOD-like receptor thermal protein domain associated protein 3 (NLRP3) and myeloid differentiation factor 88 (MyD88) in brain tissues. The results showed that all three postbiotics could significantly improve the learning and memory capacities of AD rats, significantly reduce the content of Aβ in hippocampal tissues, and decrease the LPS levels in feces, serum, and hippocampal tissues and the relative mRNA transcription levels of TLR4, NLRP3 and MyD88 in brain tissues. Intervention with the postbiotics regulated the structure and composition of the intestinal microbiota. In the postbiotic intervention groups, the relative abundance of the predominant intestinal bacteria, Firmicutes, and the beneficial species, Ruminococcaceae increased, the relative abundance of the potential harmful intestinal bacteria, Muribaculaceae, decreased compared with the AD model group. Thus, the postbiotics IOBL07, IOB602, and IOB413 have significant efficacy in ameliorating memory and cognitive deficits in AD rats, the most pronounced effect being observed with high-dose IOB602. The underlying mechanisms might be associated with regulating the structure and composition of the gut microbiota and down-regulating the relative mRNA transcription levels of TLR4, NLRP3 and MyD88 in brain tissues.

Chronic kidney disease (CKD) is one kind of illness with abnormal renal structure and function caused by many factors. Probiotics can be used to regulate intestinal microflora and enhance intestinal mucosal barrier, thus, intervention with probiotics may be regarded as one of the potential ways to protect against CKD. In vitro and in vivo experiments showed that Lactiplantibacillus plantarum MA2 (MA2), a probiotic separated from traditional Chinese Tibetan kefir grains, could degrade the uremic toxins including creatinine, urea nitrogen and uric acid. Oral administration of MA2 or its inactive strains (IMA2) could decrease serum uremic toxins of adenine-induced CKD mice, and also elevate the relative expression of claudin-1. Meanwhile, intervention of MA2 or IMA2 decreased the contents of lipopolysaccharide, Toll-like receptor 4 (TLR4) and interleukin-1β (IL-1β) in the kidney. 16S rDNA sequencing results indicated that the intervention of MA2 or IMA2 regulated the gut microbiota structure by elevating the abundance of Lactobacillus, and decreasing the abundance of Proteobacteria. Thus, oral administration of MA2 or IMA2 can reduce the uremic toxins in CKD mice by regulating gut microflora and restoring the intestinal mucosal barrier. Our study provided a theoretical basis for the application of MA2 and its postbiotics in the CKD intervention and treatment.