Department of Experimental and Clinic Medicine, Section of Psychiatry, University of Pisa, Via Roma 67, 56100, Pisa, Italy.
Department of Neuroscience and Rehabilitation, Section of Psychiatry, University of Ferrara, Italy.
Curr Med Chem. 2022;29(35):5595-5605. doi: 10.2174/0929867328666211214164907.
Since insomnia and disturbed sleep may affect neuroplasticity, we aimed at reviewing their potential role as markers of disrupted neuroplasticity involved in mood disorders.
We performed a systematic review, according to PRIMA, on PubMed, PsycINFO and Embase electronic databases for literature regarding mood disorders, insomnia, sleep loss/deprivation in relation to different pathways involved in the impairment of neuroplasticity in mood disorders such as (1) alterations in neurodevelopment (2) activation of the stress system (3) neuroinflammation (4) neurodegeneration/neuroprogression, (5) deficit in neuroprotection.
Sixty-five articles were analyzed and a narrative/ theoretical review was conducted. Studies showed that insomnia, sleep loss and sleep deprivation might impair brain plasticity of those areas involved in mood regulation throughout different pathways. Insomnia and disrupted sleep may act as neurobiological stressors by over-activating the stress and inflammatory systems, which may affect neural plasticity causing neuronal damage. In addition, disturbed sleep may favor a deficit in neuroprotection hence contributing to impaired neuroplasticity.
Insomnia and disturbed sleep may play a role as markers of alteration in brain plasticity in mood disorders. Assessing and targeting insomnia in the clinical practice may potentially play a neuroprotective role, contributing to "repairing" alterations in neuroplasticity or to the functional recovery of those areas involved in mood and emotion regulation.
由于失眠和睡眠障碍可能会影响神经可塑性，我们旨在综述它们作为与心境障碍相关神经可塑性障碍有关的生物标志物的潜在作用。
我们按照 PRIMA 指南，在 PubMed、PsycINFO 和 Embase 电子数据库中对与心境障碍、失眠、睡眠缺失/剥夺相关的文献进行了系统性综述，这些文献涉及到神经可塑性障碍的不同途径，如：（1）神经发育改变；（2）应激系统激活；（3）神经炎症；（4）神经退行性变/神经进展；（5）神经保护不足。
分析了 65 篇文章，并进行了叙述性/理论性综述。研究表明，失眠、睡眠缺失和睡眠剥夺可能通过不同途径损害与情绪调节相关的大脑可塑性。失眠和睡眠障碍可能通过过度激活应激和炎症系统作为神经生物学应激源，从而影响神经可塑性，导致神经元损伤。此外，睡眠障碍可能导致神经保护不足，从而影响神经可塑性。
失眠和睡眠障碍可能作为心境障碍中大脑可塑性改变的标志物发挥作用。在临床实践中评估和治疗失眠可能具有神经保护作用，有助于“修复”神经可塑性的改变，或恢复与情绪和情感调节相关的区域的功能。
