Research press release


Nature Neuroscience

Protein involved in Alzheimer's disease may disrupt sleep-associated memory in healthy older adults


Matthew Walkerたちは、70歳から79歳の健常成人26人について、一晩の睡眠前後で対にした単語を思い出す能力を研究した。睡眠中の被験者の脳波を記録し、誘導fMRIとPETスキャンにかけた。研究の結果、内側前頭前皮質という脳領域にAβが過剰に蓄積していると、ノンレム(非 急速眼球運動、NREM)睡眠時の脳の徐波活動が減少する状態と記憶障害の増加を予測できた。Walkerたちは、こうした蓄積がNREM睡眠時の脳の徐波活動を乱し、Aβの誘導する撹乱がひいては長期記憶の固定を直接損なうことを示唆している。


Disruption in sleep-associated memory consolidation is associated with the accumulation of β-amyloid (Aβ) in the prefrontal cortex of healthy older adults, reports a paper in Nature Neuroscience. Accumulation of Aβ is already a leading candidate mechanism for memory impairment in aging and Alzheimer’s disease, and this research highlights a possible role for cognitive decline related to sleep disruption in healthy aging.

Matthew Walker and colleagues studied the ability of 26 healthy adults, between ages 70 and 79, to remember word pairs before and after a night’s sleep. They recorded the brain waves of participants during sleep, in addition to conducting fMRI and PET scans. Their research shows that the extent of Aβ accumulation in a brain region called the medial prefrontal cortex predicts a reduction in slow wave brain activity during non-rapid eye movement (NREM) sleep and an increase in memory impairments. The authors suggest that this accumulation disrupts slow wave brain activity during NREM sleep and that this Aβ-induced disruption, in turn, directly impairs long-term memory consolidation.

While this study cannot attribute Aβ accumulation as the causative factor in disruption of NREM sleep and memory decline, it highlights sleep disruption as an important factor contributing to cognitive decline and raises the possibility of exploring therapeutic sleep intervention to mitigate age-related cognitive decline associated with Aβ pathology.

doi: 10.1038/nn.4035

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