increased levels of Aβ triggered by SCFA in vivo are not mediated by major quantitative or qualitative changes in Aβ production
通过测定一系列与Aβ产生有关的蛋白和合成过程蛋白（APP C端片段C83和C99、负责APP加工的分泌酶(BACE1, ADAM10和γ-分泌酶PSEN1的催化亚基)的蛋白水平、体外细胞添加SCFA后的γ分泌酶活性），确定SCFA不改变Aβ生成，因此推断改变的是沉积和清除过程。
(Fig. 1D).
高浓度丁酸钠（5mM）对B10细胞有明显的诱导凋亡作用；而在0.5mM时有最强的诱导效率，尽管也有一些抑制增殖效果，但不引起凋亡
conversion of microglia from proinflammatory profile to anti-inflammatory profile was associated with the inhibition of NF-κB signaling
阅读原文：
mouse primary microglia cells
学习处理原代小胶的实验方法
butyrate treatment suppressed the phosphorylation of NF-κB p65.
从小胶活化和COX-2表达变化，怎么到NF-κB -65水平的？逻辑链？
Figure 4
学习菌群测序的图表内容，做一张图
Images are representative of FJC staining,
退变神经元染色：FJC
Aβ-induced BV2 microglia are pretreated with butyrate
学习细胞实验的方法和实验参数
Discussion
用脑内注射Aβ的形式造模，分组有：伪手术组，AD组（双歧杆菌口服、对照、双歧杆菌死细菌结构口服、乙酸水溶液四种治疗组）。观察到活双歧杆菌能够改善小鼠由Aβ引起的认知障碍，健康组和AD组海马RNA表达有明显差异，而AD治疗组和对照组没有明显差异，说明治疗作用是间接的。进一步研究双歧杆菌治疗对乙酸水平的影响，发现不同方法提高乙酸水平后确实有一定疗效，提示这一过程是通过乙酸为媒介实现的。具体机制还未明。
SCFAs significantly improve cognition in AD, the pathologies of Aβ and tau, and neuroinflammation, suggesting that they have potential value in the treatment of AD. At present, the regulation of SCFA concentrations in the body is divided mainly into three types. First, the in vivo concentration of SCFAs can be regulated by oral or intravenous supplementation of SCFAs, as summarized above. The second approach is to rebuild a healthy homeostatic system of gut microbes through fecal transplants or probiotics [161]. For example, oral administration of Bifidobacterium breve strain A1, which can produce acetate, significantly ameliorated Aβ-induced cognitive impairment [162]. Clostridium butyricum, which produces butyrate, can ameliorate cognitive impairment, reduce Aβ deposition, and inhibit neuroinflammation by reducing both microglial activation and secretion of proinflammatory cytokines [148]. In addition, transplantation of wild-type mouse feces into APP/PS1 mice can improve pathological indicators by increasing the production of SCFAs [163]. The proportions of metabolic substrates that are converted into the corresponding SCFAs can be increased by adjusting the diet, including consuming prebiotics or a healthy diet [164]. It was recently reported in patients with mild cognitive impairment that a modified Mediterranean-ketogenic diet increases fecal propionate and butyrate levels, which are negatively correlated with Aβ-42 [165].
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