Therapeutic potential of Bifidobacterium breve strain A1 for preventing cognitive impairment in Alzheimer\u2019s disease

Yodai Kobayashi,Hirosuke Sugahara,Takashi Kondo,Kousuke Shimada,Keiko Abe,Jin-Zhong Xiao,Tetsuya Kuhara,Eri Mitsuyama,Akihito Yasuoka

doi:10.1038/s41598-017-13368-2

Abstract

It has previously been shown that the consumption of probiotics may have beneficial effects not only on peripheral tissues but also on the central nervous system and behavior via the microbiota–gut–brain axis, raising the possibility that treatment with probiotics could be an effective therapeutic strategy for managing neurodegenerative disorders. In this study, we investigated the effects of oral administration of Bifidobacterium breve strain A1 (B. breve A1) on behavior and physiological processes in Alzheimer’s disease (AD) model mice. We found that administration of B. breve A1 to AD mice reversed the impairment of alternation behavior in a Y maze test and the reduced latency time in a passive avoidance test, indicating that it prevented cognitive dysfunction. We also demonstrated that non-viable components of the bacterium or its metabolite acetate partially ameliorated the cognitive decline observed in AD mice. Gene profiling analysis revealed that the consumption of B. breve A1 suppressed the hippocampal expressions of inflammation and immune-reactive genes that are induced by amyloid-β. Together, these findings suggest that B. breve A1 has therapeutic potential for preventing cognitive impairment in AD.

Highlights

Alzheimer’s disease (AD) is characterized pathologically by the accumulation of neurofibrillary tangles of hyperphosphorylated tau and senile plaques that are mainly composed of amyloid-β (Aβ)[1]
We investigated the effect of Bifidobacterium breve strain A1 (B. breve A1) on the behaviors and physiological processes of AD model mice
There was no significant difference in the total number of entries into the three arms among the groups except for the donepezil group (Fig. 1c), suggesting that B. breve A1 did not affect locomotor activity

Summary

Introduction

AD is characterized pathologically by the accumulation of neurofibrillary tangles of hyperphosphorylated tau and senile plaques that are mainly composed of amyloid-β (Aβ)[1]. Disease progression is too advanced for treatment once AD has become clinically obvious. This highlights the importance of preventing the onset of AD through improvements in lifestyle or diet[5]. It has been reported that consumption of a mixture of probiotics could affect cognitive function and some metabolic statuses in AD patients[15]. We investigated the effect of Bifidobacterium breve strain A1 (B. breve A1) on the behaviors and physiological processes of AD model mice. We found that this probiotic can prevent the cognitive dysfunction induced by Aβ, indicating its therapeutic potential in AD patients

Methods

Results

Conclusion