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热量限制导致实验性阿尔茨海默病的减弱是由于肠道微生物组的改变。

Caloric restriction leading to attenuation of experimental Alzheimer's disease results from alterations in gut microbiome.

机构信息

Department of Neurology, The Affiliated Brain Hospital, Guangzhou Medical University, Guangzhou, China.

Guangdong Yunzhao Medical Technology Co., Ltd., Guangzhou, China.

出版信息

CNS Neurosci Ther. 2024 Jul;30(7):e14823. doi: 10.1111/cns.14823.

DOI:10.1111/cns.14823
PMID:38992870
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11239325/
Abstract

BACKGROUND

Caloric restriction (CR) might be effective for alleviating/preventing Alzheimer's disease (AD), but the biological mechanisms remain unclear. In the current study, we explored whether CR caused an alteration of gut microbiome and resulted in the attenuation of cognitive impairment of AD animal model.

METHODS

Thirty-week-old male APP/PS1 transgenic mice were used as AD models (AD mouse). CR was achieved by 30% reduction of daily free feeding (ad libitum, AL) amount. The mice were fed with CR protocol or AL protocol for six consecutive weeks.

RESULTS

We found that with CR treatment, AD mice showed improved ability of learning and spatial memory, and lower levels of Aβ40, Aβ42, IL-1β, TNF-α, and ROS in the brain. By sequencing 16S rDNA, we found that CR treatment resulted in significant diversity in composition and abundance of gut flora. At the phylum level, Deferribacteres (0.04%), Patescibacteria (0.14%), Tenericutes (0.03%), and Verrucomicrobia (0.5%) were significantly decreased in CR-treated AD mice; at the genus level, Dubosiella (10.04%), Faecalibaculum (0.04%), and Coriobacteriaceae UCG-002 (0.01%) were significantly increased in CR-treated AD mice by comparing with AL diet.

CONCLUSIONS

Our results demonstrate that the attenuation of AD following CR treatment in APP/PS1 mice may result from alterations in the gut microbiome. Thus, gut flora could be a new target for AD prevention and therapy.

摘要

背景

热量限制（CR）可能对缓解/预防阿尔茨海默病（AD）有效，但生物学机制尚不清楚。在本研究中，我们探讨了 CR 是否引起肠道微生物组的改变，从而导致 AD 动物模型认知障碍的减弱。

方法

30 周龄雄性 APP/PS1 转基因小鼠被用作 AD 模型（AD 小鼠）。CR 通过每日自由喂养（AL）量减少 30%来实现。这些小鼠连续六周接受 CR 方案或 AL 方案喂养。

结果

我们发现，经过 CR 治疗，AD 小鼠的学习和空间记忆能力得到改善，大脑中的 Aβ40、Aβ42、IL-1β、TNF-α 和 ROS 水平降低。通过测序 16S rDNA，我们发现 CR 治疗导致肠道菌群组成和丰度发生显著变化。在门水平上，Deferribacteres（0.04%）、Patescibacteria（0.14%）、Tenericutes（0.03%）和 Verrucomicrobia（0.5%）在 CR 治疗的 AD 小鼠中显著减少；在属水平上，Dubosiella（10.04%）、Faecalibaculum（0.04%）和 Coriobacteriaceae UCG-002（0.01%）在 CR 治疗的 AD 小鼠中显著增加与 AL 饮食相比。

结论

我们的结果表明，APP/PS1 小鼠 CR 治疗后 AD 的减弱可能是由于肠道微生物组的改变所致。因此，肠道菌群可能成为 AD 预防和治疗的新靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9915/11239325/e644bdff7289/CNS-30-e14823-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9915/11239325/9435a24456f7/CNS-30-e14823-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9915/11239325/328c6edef964/CNS-30-e14823-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9915/11239325/f7b76d89f01d/CNS-30-e14823-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9915/11239325/d6541e3355dc/CNS-30-e14823-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9915/11239325/a6258a438e3c/CNS-30-e14823-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9915/11239325/69bad8c96085/CNS-30-e14823-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9915/11239325/97ac97a6ec55/CNS-30-e14823-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9915/11239325/6a26c0788d96/CNS-30-e14823-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9915/11239325/de92288e28c6/CNS-30-e14823-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9915/11239325/e644bdff7289/CNS-30-e14823-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9915/11239325/9435a24456f7/CNS-30-e14823-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9915/11239325/328c6edef964/CNS-30-e14823-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9915/11239325/f7b76d89f01d/CNS-30-e14823-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9915/11239325/d6541e3355dc/CNS-30-e14823-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9915/11239325/a6258a438e3c/CNS-30-e14823-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9915/11239325/69bad8c96085/CNS-30-e14823-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9915/11239325/97ac97a6ec55/CNS-30-e14823-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9915/11239325/6a26c0788d96/CNS-30-e14823-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9915/11239325/de92288e28c6/CNS-30-e14823-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9915/11239325/e644bdff7289/CNS-30-e14823-g010.jpg

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