休斯顿卫理公会医院的研究人员揭示了肥胖与阿尔茨海默病之间的生物学机制。[1]研究由Stephen Wong博士和Li Yang博士共同领导，发表在《分子神经变性》期刊上。[1]研究发现，肥胖会导致磷脂酰乙醇胺（PEs）这类脂肪分子水平升高，这些分子能进入大脑，削弱免疫防御并促进淀粉样蛋白积累。[1]
根据美国疾病控制与预防中心的数据，目前超过650万美国人患有阿尔茨海默病，预计到2060年这一数字将增至近1400万。[1]Stephen Wong博士表示："肥胖可以改变信号如何传到大脑。好消息是这可能是我们可以治疗的东西。"[1]研究显示，恢复磷脂酰乙醇胺的健康平衡改善了阿尔茨海默病模型的脑功能和认知表现。[1]
Researchers at Houston Methodist have identified a mechanism by which obesity may contribute to Alzheimer's disease development.[1] The study, led by Dr. Stephen Wong and Dr. Li Yang, found that obesity elevates levels of phosphatidylethanolamines (PEs), a class of fatty molecules that can cross into the brain, compromise immune defenses, and promote the accumulation of amyloid protein.[1] According to Dr. Wong, "Obesity can alter how signals are transmitted to the brain. The encouraging aspect is that this may represent something we can treat."[1]
The research, published in Molecular Neurodegeneration in 2026, demonstrated that restoring healthy PE balance improved brain function and cognitive performance in Alzheimer's disease models.[1] This finding offers potential therapeutic avenues for a condition affecting more than 6.5 million Americans currently, with projections indicating the number could reach nearly 14 million by 2060 according to data from the Centers for Disease Control and Prevention.[1]