Sleep disturbances in Alzheimer's and Parkinson's diseases.
Sleep disturbances in Alzheimer's and Parkinson's diseases.
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DOI：
10.1007/s12017-012-8181-2
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发表时间：
2012-09
影响因子：
3.5
通讯作者：
Mattson MP
中科院分区：
文献类型：
--
作者：
Rothman SM;Mattson MP
阿尔茨海默病（AD）和帕金森病（PD）是两种最常见的神经退行性疾病，对我们的社会造成的负担超过了心血管疾病和癌症的总和。虽然认知和运动症状分别用于定义AD和PD，但患有这两种疾病的患者表现出睡眠障碍，包括失眠、嗜睡和过度白天小睡。AD和PD患者睡眠紊乱的分子基础可能涉及控制睡眠-觉醒周期的下丘脑和脑干核团的损伤。神经递质和激素信号传导的扰动（例如，血清素、去甲肾上腺素和褪黑激素）和神经营养因子BDNF可能有助于疾病过程。神经毒性形式的淀粉样β-肽、tau和α-突触核蛋白的异常积累发生在AD和PD患者中参与睡眠调节的脑区域中，并且足以在这些神经退行性疾病的动物模型中引起睡眠障碍。睡眠调节紊乱通常发生在AD和PD病程的早期，并可能导致认知和运动症状。针对控制睡眠的信号通路的治疗已被证明可以延缓AD和PD动物模型中的疾病进程，这表明在这些疾病的风险或早期阶段的人类中进行此类干预的潜力。
Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the two most common neurodegenerative disorders, and exact a burden on our society greater than cardiovascular disease and cancer combined. While cognitive and motor symptoms are used to define AD and PD, respectively, patients with both disorders exhibit sleep disturbances including insomnia, hypersomnia and excessive daytime napping. The molecular basis of perturbed sleep in AD and PD may involve damage to hypothalamic and brainstem nuclei that control sleep – wake cycles. Perturbations in neurotransmitter and hormone signaling (e.g., serotonin, norepinephrine and melatonin) and the neurotrophic factor BDNF likely contribute to the disease process. Abnormal accumulations of neurotoxic forms of amyloid β-peptide, tau and α-synuclein occur in brain regions involved in the regulation of sleep in AD and PD patients, and are sufficient to cause sleep disturbances in animal models of these neurodegenerative disorders. Disturbed regulation of sleep often occurs early in the course of AD and PD, and may contribute to the cognitive and motor symptoms. Treatments that target signaling pathways that control sleep have been shown to retard the disease process in animal models of AD and PD, suggesting a potential for such interventions in humans at risk for, or in the early stages of these disorders.