Larouche Eddy, Hudon Carol, Goulet Sonia
École de psychologie, Université Laval, 2325, rue des Bibliothèques, Québec, QC, Canada G1V 0A6; Centre de recherche de l'Institut universitaire en santé mentale de Québec (CRIUSMQ), 2601, de la Canardière (F-2400), Québec, QC, Canada G1J 2G3.
École de psychologie, Université Laval, 2325, rue des Bibliothèques, Québec, QC, Canada G1V 0A6; Centre de recherche de l'Institut universitaire en santé mentale de Québec (CRIUSMQ), 2601, de la Canardière (F-2400), Québec, QC, Canada G1J 2G3.
Behav Brain Res. 2015 Jan 1;276:199-212. doi: 10.1016/j.bbr.2014.05.058. Epub 2014 Jun 2.
The present article is based on the premise that the risk of developing Alzheimer's disease (AD) from its prodromal phase (mild cognitive impairment; MCI) is higher when adverse factors (e.g., stress, depression, and metabolic syndrome) are present and accumulate. Such factors augment the likelihood of hippocampal damage central in MCI/AD aetiology, as well as compensatory mechanisms failure triggering a switch toward neurodegeneration. Because of the devastating consequences of AD, there is a need for early interventions that can delay, perhaps prevent, the transition from MCI to AD. We hypothesize that mindfulness-based interventions (MBI) show promise with regard to this goal. The present review discusses the associations between modifiable adverse factors and MCI/AD decline, MBI's impacts on adverse factors, and the mechanisms that could underlie the benefits of MBI. A schematic model is proposed to illustrate the course of neurodegeneration specific to MCI/AD, as well as the possible preventive mechanisms of MBI. Whereas regulation of glucocorticosteroids, inflammation, and serotonin could mediate MBI's effects on stress and depression, resolution of the metabolic syndrome might happen through a reduction of inflammation and white matter hyperintensities, and normalization of insulin and oxidation. The literature reviewed in this paper suggests that the main reach of MBI over MCI/AD development involves the management of stress, depressive symptoms, and inflammation. Future research must focus on achieving deeper understanding of MBI's mechanisms of action in the context of MCI and AD. This necessitates bridging the gap between neuroscientific subfields and a cross-domain integration between basic and clinical knowledge.
在前驱期(轻度认知障碍;MCI)发展为阿尔茨海默病(AD)的风险,在存在并累积不利因素(如压力、抑郁和代谢综合征)时会更高。这些因素增加了海马体损伤的可能性,而海马体损伤是MCI/AD病因的核心,同时也增加了代偿机制失效从而引发向神经退行性变转变的可能性。由于AD的破坏性后果,需要早期干预措施来延缓,甚至可能预防从MCI向AD的转变。我们假设基于正念的干预措施(MBI)在实现这一目标方面具有前景。本综述讨论了可改变的不利因素与MCI/AD病情恶化之间的关联、MBI对不利因素的影响,以及MBI产生益处的潜在机制。本文提出了一个示意图模型,以说明MCI/AD特有的神经退行性变过程,以及MBI可能的预防机制。糖皮质激素、炎症和血清素的调节可能介导MBI对压力和抑郁的影响,而代谢综合征的缓解可能是通过减轻炎症和白质高信号、使胰岛素和氧化正常化来实现的。本文综述的文献表明,MBI对MCI/AD发展的主要作用涉及压力、抑郁症状和炎症的管理。未来的研究必须专注于更深入地了解MBI在MCI和AD背景下的作用机制。这需要弥合神经科学子领域之间的差距,并实现基础与临床知识的跨领域整合。