Protective Effects of Bacillus coagulans JA845 against D-Galactose/AlCl3-Induced Cognitive Decline, Oxidative Stress and Neuroinflammation

Recently, the efficacy of probiotics in treatment of neurodegenerative disorders has been reported in animal and clinical studies. Here, we assessed the effects of Bacillus coagulans JA845 in counteracting the symptoms of D-galactose (D-gal)/AlCl3-induced Alzheimer's disease (AD) in a mice model through behavioral test, histological assessment and biochemical analysis. Ten weeks of pretreatment with B. coagulans JA845 prevented cognitive decline, attenuated hippocampal lesion and protected neuronal integrity, which demonstrated the neuroprotective features of B. coagulans JA845 in vivo. We also found that supplementation of B. coagulans JA845 alleviated amyloid-beta deposits and hyperphosphorylated tau in hippocampus of D-gal/AlCl3-induced AD model mice. Furthermore, B. coagulans JA845 administration attenuated oxidative stress and decreased serum concentration of inflammatory cytokines by regulating the Nrf2/HO-1 and MyD88/TRAF6/NF-kappa B pathway. Our results demonstrated for the first time that B. coagulans has the potential to help prevent cognitive decline and might be a novel therapeutic approach for the treatment of neurodegenerative diseases.

Automated summary

The study found that B. coagulans JA845 can prevent cognitive decline and protect neuronal integrity in a mouse model of AD. In addition, it can reduce amyloid-beta deposits and hyperphosphorylated tau, as well as attenuate oxidative stress and decrease inflammatory cytokines through the regulation of Nrf2/HO-1 and MyD88/TRAF6/NF-kappa B pathway.