Cruz-Aguilar Manuel Alejandro, Ramírez-Salado Ignacio, Guevara Miguel Angel, Hernández-González Marisela, Benitez-King Gloria
Universidad de Guadalajara, Instituto de Neurociencias, CUCBA, Laboratorio de Correlación Electroencefalográfica y Conducta, Guadalajara, Jalisco, México.
Instituto Nacional de Psiquiatría "Ramón de la Fuente Muñiz", Dirección de Investigaciones en Neurociencias, Laboratorio de Cronobiología y Sueño, CDMX, México.
J Alzheimers Dis Rep. 2018 Mar 6;2(1):55-65. doi: 10.3233/ADR-170019.
There is evidence demonstrating that 5-mg of fast-release melatonin significantly reduces nocturnal sleep onset in patients with mild-to-moderate Alzheimer's disease (AD). However, the physiological mechanism that could promote sleep installation by melatonin in patients with AD is still poorly understood. The present pilot study was designed to analyze the effects of melatonin on cortical activity during the sleep onset period (SOP) in eight mild-to-moderate AD patients treated with 5-mg of fast-release melatonin. Electroencephalographic recordings were obtained from C3-A1, C4-A2, F7-T3, F8-T4, F3-F4, and O1-O2. The relative power (RP), interhemispheric, intrahemispheric, and fronto-posterior correlations of six electroencephalographic bands were calculated and compared between two conditions: placebo and melatonin. Results show that at F7-T3, F3-F4, and C3-A1, melatonin induced an increase of the RP of the delta band. Likewise, in F7-T3, melatonin induced a decrease of the RP in the alpha1 band. Similarly, results show a lower interhemispheric correlation between the F7-T3 and F8-T4 derivations in the alpha1 band compared to the placebo condition. We conclude that the short sleep onset related to melatonin intake in AD patients was associated with a lower RP of the alpha1, a higher RP of the delta band (mainly in the left hemisphere) and a decreased interhemispheric EEG coupling in the alpha1 band. The possible role of the GABAergic neurotransmission as well as of the cascade of neurochemical events that melatonin triggers on sleep onset are discussed.
有证据表明，5毫克速释褪黑素可显著缩短轻度至中度阿尔茨海默病（AD）患者的夜间入睡时间。然而，褪黑素促进AD患者入睡的生理机制仍知之甚少。本初步研究旨在分析5毫克速释褪黑素治疗的8例轻度至中度AD患者在入睡期（SOP）褪黑素对皮质活动的影响。脑电图记录取自C3-A1、C4-A2、F7-T3、F8-T4、F3-F4和O1-O2。计算并比较了安慰剂和褪黑素两种情况下六个脑电图波段的相对功率（RP）、半球间、半球内和前后相关性。结果显示，在F7-T3、F3-F4和C3-A1处，褪黑素使δ波段的RP增加。同样，在F7-T3处，褪黑素使α1波段的RP降低。类似地，结果显示，与安慰剂组相比，α1波段F7-T3和F8-T4导联之间的半球间相关性更低。我们得出结论，AD患者摄入褪黑素后入睡时间缩短与α1波段较低的RP、δ波段较高的RP（主要在左半球）以及α1波段半球间脑电图耦合降低有关。文中讨论了γ-氨基丁酸能神经传递以及褪黑素引发的神经化学事件级联在入睡过程中的可能作用。
