Gut Dysbiosis Activates C/EBPβ/AEP Pathway in Alzheimer’s Disease Mouse Model

Kaihua Li

doi:10.54097/pgz02551

Authors

Kaihua Li

DOI:

https://doi.org/10.54097/pgz02551

Keywords:

Gut dysbiosis; Alzheimer’s disease; C/EBPβ/AEP; BDNF; treatments.

Abstract

The mechanisms of developing Alzheimer’s disease (AD) under the influence of gut microbial composition are intensively studied currently. However, the specific mechanism remains unknown. One recent study conducted by Chen et al. provided a breakthrough for the underlying mechanism of gut dysbiosis in contributing to the disease and showed the efficacy of two potential treatments in mouse models. Based on their study, gut dysbiosis occurred in transgenic mice increased the C/EBPβ/AEP signaling of the brain and the gut as aging, which increased the amount of truncated β-amyloid precursor protein and Tau. And the level of brain-derived neurotropic factor or BDNF was reduced significantly in the gut and the brain of aged transgenic mice. It implied that both genetic and gut microbial composition play roles in developing Alzheimer’s disease. Besides, antibiotic treatments and prebiotic R13 were performed. Researcher mitigated the pathologies and phenotypical symptoms. But only R13 treatment upregulated BDNF in the brain. Some experimental methods of the study could be improved to provide more useful information including the effect in female mice. In general, the original paper provided a logical procedure or outline for the study and introduced promising treatments in AD. Some questions remain including the mechanism of gut microbiota alteration in mediating the gut and the brain BDNF production is unclear. Based on this, hypothetical experiments are designed in the review.

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