Saccharomyces boulardii ameliorates gut dysbiosis associated cognitive decline
Authors: Kaberi Chatterjee
Sugato Banerjee
Maria Adhikary
Suparna Roy Sarkar
Kunal Mukhopadhyay
Papiya Mitra Mazumder
Abhishek Sarkar
Journal: Physiology & Behavior (2021)
Discipline: NEUROSCIENCE & BEHAVIOR
Keywords: Cognition; Gut dysbiosis; Gut microbiota; S. boulardii.
Affiliations: Department of Pharmaceutical Sciences and Technology, Birla Institute of Technology, Mesra, Ranchi, Jharkhand, India., Department of Bioengineering, Birla Institute of Technology, Mesra, Ranchi, Jharkhand, India., Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, Kolkata, West Bengal, India. Electronic address: .

Abstract:  Saccharomyces boulardii, a probiotic yeast is well prescribed for various gastrointestinal disorders accompanied by gut dysbiosis such as inflammatory bowel disease, bacterial diarrhea and antibiotic associated diarrhea. Gut dysbiosis has been associated with central nervous system via gut brain axis primarily implied in the modulation of psychiatric conditions. In the current study we use Saccharomyces boulardii as a therapeutic agent against gut dysbiosis associated cognitive decline. In mice, gut dysbiosis was induced by oral Ampicillin Na (250 mg/kg twice-daily) for 14 days. While in the treatment group S. boulardii (90 mg/kg once a day) was administered orally for 21 days along with 14 days of antibiotic treatment. Gene expression studies revealed antibiotic mediated decrease in the Lactobacillus, Bifidobacterium, Firmicutes and Clostridium which were restored by S. boulardii treatment. Cognitive behavioral studies showed a parallel reduction in fear conditioning, spatial as well as recognition memory which were reversed upon S. boulardii treatment in these animals. S. boulardii treatment reduced myeloperoxidase enzyme, an inflammatory marker, in colon as well as brain which was increased after antibiotic administration. Similarly, S. boulardii reduced the brain acetylcholine esterase, oxidative stress and inflammatory cytokines and chemokines which were altered due to antibiotic treatment. S. boulardii treatment also protected hippocampal neuronal damage and restored villus length and crypt depth thus normalizing gut permeability in antibiotic treated animals. Hence, we conclude that S. boulardii prevented antibiotic associated gut dysbiosis leading to reduced intestinal and brain inflammation and oxidative stress thus preventing hippocampal neuronal damage and eventually reversing gut dysbiosis associate cognitive decline in mice. 

Retracted: No

PubPeer comments:
 I read this paper with great interest. At first I was striked by the marked phenotype caused by low-dose antibiotics administration. To my knowledge, a 50% reduction of hippocampal neurons after antibiotherapy has never been described, although the medication has been widely used in clinic and in animal models for decades. Effect of antibiotics on other readouts is also intriguing but not as much as the spectacular reversion of the phenotype upon probiotic administration, at a low dose of course. Then I came across this other paper sharing some authors and describing the exact same effect of a different probiotic on antibiotics-induced cognitive decline : https: doi.org 10.1016 j.jneuroim.2020.577390 Here is figure 2 of the two papers, side by side ![file] Fig 3 ![file] Fig 4 ![file] Fig 7 8 ![file] Could the authors explain how they managed to get such reproducible effects on the exact same readouts using two different probiotics, allowing to publish two almost identical papers sharing the same structure and organization ? Thank you ,