Universidade de São Paulo - Faculdade de Medicina, R. Dr.Enéas de Carvalho Aguiar, 255, São Paulo (SP), Brazil.
Universidade Federal de São Paulo - Escola Paulista de Medicina, R. Botucatu, 862, São Paulo (SP), Brazil.
Sleep Med. 2024 Sep;121:359-364. doi: 10.1016/j.sleep.2024.07.028. Epub 2024 Jul 24.
Few studies have assessed whether neuropathological markers of AD in the preclinical and prodromal stages are associated with polysomnographic changes and obstructive sleep apnea (OSA).
This was a cross-sectional, case-control study of older adults (≥60 years) without relevant clinical and psychiatric comorbidities selected randomly from a cohort of individuals without dementia in a tertiary university hospital in São Paulo, Brazil. They underwent neuropsychological evaluation for clinical diagnosis and were allocated into two samples: cognitively unimpaired (CU) and mild cognitive impairment (MCI). Also, they underwent PET-PiB to determine the amyloid profile and all-night in-lab polysomnography. For each sample, we compared polysomnographic parameters according to the amyloid profile (A+ vs A-).
We allocated 67 participants (mean age 73 years, SD 10,1), 70 % females, 14 ± 5 years of education, into two samples: CU (n = 28, 42.4 %) and MCI (n = 39, 57.6 %). In the CU sample, the group A+ (n = 9) showed worse sleep parameters than A- (n = 19) (lower total sleep time (p = 0.007), and sleep efficiency (p = 0.005); higher sleep onset latency (p = 0.025), wake time after sleep onset (p = 0.011), and arousal index (AI) (p = 0.007)), and changes in sleep structure: higher %N1 (p = 0.005), and lower %REM (p = 0.006). In the MCI sample, MCI A-had higher AI (p = 0.013), respiratory disturbance index (p = 0.025, controlled for age), and higher rates of severe OSA than A+.
The amyloid profile was associated with polysomnographic markers of worse sleep quality in individuals with preclinical AD but not with prodromal AD, probably due to the higher frequencies of severe OSA.
很少有研究评估 AD 的神经病理学标志物在临床前和前驱期是否与多导睡眠图变化和阻塞性睡眠呼吸暂停（OSA）有关。
这是一项在巴西圣保罗的一家三级大学医院的无痴呆队列中随机选择的无相关临床和精神共病的老年（≥60 岁）成年人的横断面、病例对照研究。他们接受神经心理学评估以进行临床诊断，并分为两个样本：认知正常（CU）和轻度认知障碍（MCI）。此外，他们还接受了 PET-PiB 以确定淀粉样蛋白谱和整夜实验室多导睡眠图。对于每个样本，我们根据淀粉样蛋白谱（A+与 A-）比较了多导睡眠图参数。
我们将 67 名参与者（平均年龄 73 岁，标准差 10.1）、70%为女性、14±5 年教育程度分配到两个样本：CU（n=28，42.4%）和 MCI（n=39，57.6%）。在 CU 样本中，A+组（n=9）的睡眠参数比 A-组（n=19）差（总睡眠时间更低（p=0.007），睡眠效率更低（p=0.005）；睡眠潜伏期更高（p=0.025），睡眠后觉醒时间更长（p=0.011），唤醒指数（AI）更高（p=0.007）），并且睡眠结构发生变化：N1%更高（p=0.005），REM%更低（p=0.006）。在 MCI 样本中，MCI A-组的 AI 更高（p=0.013），呼吸干扰指数更高（p=0.025，年龄校正后），严重 OSA 的发生率高于 A+。
淀粉样蛋白谱与临床前 AD 个体多导睡眠图的睡眠质量恶化标志物相关，但与前驱 AD 无关，可能是由于严重 OSA 的频率较高。
