哈佛医学院的研究团队在《Alzheimer's & Dementia》期刊上发表了一项出人意料的研究成果，揭示了急性肠炎对阿尔茨海默病（AD）病理的影响。研究使用5xFAD小鼠模型，通过葡聚糖硫酸钠盐（DSS）诱导急性结肠炎，发现尽管肠道微生物失衡和全身性炎症加剧，但小鼠脑内的Aβ沉积却减少，且Aβ向血液中的外流增加。这一结果与普遍认为的肠道疾病促进AD进展的观点相悖。
研究还显示，急性结肠炎导致小鼠全身炎症水平升高，内毒素和促炎性细胞因子浓度增加，同时脑内皮细胞活化，引发小胶质细胞活化及免疫细胞浸润。Tanzi团队认为，这可能表明存在除中枢神经系统免疫细胞之外的Aβ清除机制，并暗示Aβ释放到血液是对系统性炎症的反应，Aβ可能作为抗菌肽保护大脑。这项研究为理解肠道健康与AD之间的关系提供了新的视角。
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