The intertwining between epilepsy, sleep disorders and beta amyloid pathology has been progressively highlighted, as early identification and stratification of patients at high risk of cognitive decline is the need of the hour.

Modification of the sleep-wake activity, such as sleep impairment or excessive daytime sleepiness, can critically affect cerebral beta amyloid levels. Both mice models and human studies have demonstrated a substantial increase in the burden of beta amyloid pathology after sleep-deprivation, with potential negative effects partially restored by sleep recovery.

The accumulation of beta amyloid has been shown to be an early event in the course of Alzheimer’s disease dementia. Beta amyloid accumulation has been linked to epileptic seizures epileptic seizures, with beta amyloid being itself pro-epileptogenic in mice models already at oligomeric stage, well before plaque deposition. Further supporting a potential relationship between beta amyloid and epilepsy: i) seizures happen in 1 out of oofut 10 patients with Alzheimer’s disease in the prodromal stage, ii) epileptic activity accelerates cognitive decline in Alzheimer’s disease, iii) people with late-onset epilepsy present a critically high risk of developing dementia.

In this Review we highlight the role of beta amyloid as a potential shared mechanisms between sleep disorders, late-onset epilepsy, and cognitive decline.

癫痫、睡眠障碍和 β 淀粉样蛋白病理之间的相互交织已经逐渐得到强调，因为对认知能力下降高风险患者的早期识别和分层是一个小时的需要。

睡眠-觉醒活动的改变，例如睡眠障碍或白天过度嗜睡，会严重影响大脑 β 淀粉样蛋白水平。小鼠模型和人体研究都表明，睡眠剥夺后 β 淀粉样蛋白病理负担显着增加，睡眠恢复部分恢复了潜在的负面影响。

β淀粉样蛋白的积累已被证明是阿尔茨海默病痴呆过程中的早期事件。β 淀粉样蛋白的积累与癫痫发作有关，在斑块沉积之前，β 淀粉样蛋白本身在已经处于寡聚阶段的小鼠模型中是促癫痫发生的。进一步支持 β 淀粉样蛋白与癫痫之间的潜在关系：i) 10 名阿尔茨海默病前驱期患者中有 1 名癫痫发作，ii) 癫痫活动加速阿尔茨海默病的认知能力下降，iii) 患有迟发性癫痫的人患痴呆症的风险极高。

在这篇综述中，我们强调了 β 淀粉样蛋白作为睡眠障碍、迟发性癫痫和认知能力下降之间潜在共享机制的作用。