肠道微生物衍生的短链脂肪酸在阿尔茨海默病型β-淀粉样蛋白神经病理机制中的保护作用。
Protective roles of intestinal microbiota derived short chain fatty acids in Alzheimer's disease-type beta-amyloid neuropathological mechanisms.
机构信息
a Department of Neurology , Icahn School of Medicine at Mount Sinai , New York , NY , USA.
b Department of Neurology , Showa University School of Medicine , Tokyo , Japan.
出版信息
Expert Rev Neurother. 2018 Jan;18(1):83-90. doi: 10.1080/14737175.2018.1400909. Epub 2017 Nov 14.
BACKGROUND
Dietary fibers are metabolized by gastrointestinal (GI) bacteria into short-chain fatty acids (SCFAs). We investigated the potential role of these SCFAs in β-amyloid (Aβ) mediated pathological processes that play key roles in Alzheimer's disease (AD) pathogenesis.
RESEARCH DESIGN AND METHODS
Multiple complementary assays were used to investigate individual SCFAs for their dose-responsive effects in interfering with the assembly of Aβß1-40 and Aβ1-42 peptides into soluble neurotoxic Aβ aggregates.
RESULTS
We found that several select SCFAs are capable of potently inhibiting Aβ aggregations, in vitro.
CONCLUSION
Our studies support the hypothesis that intestinal microbiota may help protect against AD, in part, by supporting the generation of select SCFAs, which interfere with the formation of toxic soluble Aβ aggregates.
背景
膳食纤维被胃肠道（GI）细菌代谢为短链脂肪酸（SCFAs）。我们研究了这些 SCFAs 在β-淀粉样蛋白（Aβ）介导的病理过程中的潜在作用，这些过程在阿尔茨海默病（AD）发病机制中起关键作用。
研究设计和方法
使用多种互补的测定方法来研究单个 SCFAs 在干扰 Aββ1-40 和 Aβ1-42 肽组装成可溶性神经毒性 Aβ 聚集体方面的剂量反应效应。
结果
我们发现几种选择的 SCFAs 能够有效地抑制 Aβ 的聚集，在体外。
结论
我们的研究支持这样一种假设，即肠道微生物群可能有助于预防 AD，部分原因是支持生成特定的 SCFAs，这些 SCFAs 干扰有毒可溶性 Aβ 聚集体的形成。
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