肯塔基大学研究人员在阿尔茨海默病睡眠障碍领域取得重要发现。研究表明，导致患者睡眠丧失的主要原因是脑内过度活跃的免疫细胞（小胶质细胞），而非仅由淀粉样蛋白斑块引起1。研究团队通过临时清除患病小鼠脑内约87%的小胶质细胞，成功恢复了其每日超过两小时的睡眠时间1。值得注意的是，这一睡眠改善发生在淀粉样蛋白斑块水平未被清除的情况下1。
研究人员使用药物Pexidartinib（PLX3397）在14天内清除了约87%的小胶质细胞1。进一步分析发现，阿尔茨海默病选择性破坏非快速眼动睡眠（NREM），而这与正常衰老主要减少快速眼动睡眠（REM）的模式不同1。该研究由肯塔基大学的Shannon L. Macauley博士和Nicholas J. Constantino博士领导1，论文已发表于《阿尔茨海默病》2026年第22卷第6期1。
研究小组目前正在探索现有药物改变小胶质细胞代谢的潜力，包括糖尿病药物二甲双胍和抗癫痫药物Stiripentol1。这一发现为开发针对脑免疫细胞的新治疗靶点提供了可能1。
Researchers at the University of Kentucky have identified overactive immune cells in the brain, rather than amyloid plaques alone, as the primary driver of sleep loss in Alzheimer's disease.1 By temporarily removing approximately 87% of microglia—the brain's immune cells—from diseased mice using the drug Pexidartinib (PLX3397) over 14 days, the research team restored more than two hours of daily sleep in the animals.1 Remarkably, this sleep improvement occurred without any reduction in amyloid plaque levels, challenging conventional understanding of the disease mechanism.1
The findings, led by Dr. Shannon L. Macauley and Dr. Nicholas J. Constantino and published in Alzheimer's & Dementia (Volume 22, Issue 6, 2026), reveal that Alzheimer's disease selectively impairs non-rapid eye movement (NREM) sleep, whereas normal aging primarily reduces rapid eye movement (REM) sleep.1 The discovery opens new therapeutic avenues by identifying microglial activation as a distinct target for treatment. The research team is now investigating whether existing medications—including the diabetes drug metformin and the anti-epilepsy medication Stiripentol—can alter microglial metabolism to produce therapeutic benefits.1 The study received $287,236 in funding from the Alzheimer's Cure Fund and $250,000 from the CART Fund.1
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