{Reference Type}: Journal Article
{Title}: Bidirectional mechanism of comorbidity of depression and insomnia based on synaptic plasticity.
{Author}: Meng F;Wang L;
{Journal}: Zhong Nan Da Xue Xue Bao Yi Xue Ban
{Volume}: 48
{Issue}: 10
{Year}: 2023 Oct 28
暂无{DOI}: 10.11817/j.issn.1672-7347.2023.230082
{Abstract}: Insomnia is one of the most common accompanying symptoms of depression, with both sharing highly overlapping molecular pathways. The same pathological changes can trigger comorbidity of insomnia and depression, which further forms a vicious cycle with the involvement of more mechanisms and disease progression. Thus, understanding the potential interaction mechanisms between insomnia and depression is critical for clinical diagnosis and treatment. Comorbidity genetic factors, the hypothalamic-pituitary-adrenal axis, along with circadian rhythms of cortisol and the brain reward mechanism, are important ways in contributing to the comorbidity occurrence and development. However, owing to lack of pertinent investigational data, intricate molecular mechanisms necessitate further elaboration. Synaptic plasticity is a solid foundation for neural homeostasis. Pathological alterations of depression and insomnia may perturb the production and release of neurotransmitter, dendritic spine remodeling and elimination, which converges and reflects in aberrant synaptic dynamics. Hence, the introduction of synaptic plasticity research route and the construction of a comprehensive model of depression and insomnia comorbidity can provide new ideas for clinical depression insomnia comorbidity treatment plans.<BR>失眠是抑郁症最常见的伴随症状之一，二者具有高度重合的分子机制。通过相似的病理学改变可以引发失眠和抑郁症的共病，随着病程进展可能形成恶性循环。因此，了解失眠、抑郁症二者潜在交互机制对于临床诊疗十分重要。共病基因、下丘脑-垂体-肾上腺轴与皮质醇昼夜节律、免疫炎症、大脑奖赏机制是参与共病发生、发展的重要途径，但由于缺乏相关研究数据，详细的分子机制有待进一步阐明。突触可塑性是神经功能稳定的坚实基础，抑郁症和失眠的病理改变都可能影响神经递质的产生和释放、树突棘剪切和消除等过程，表现为异常的突触活动。探究突触可塑性研究路径并构建抑郁症和失眠共病发生及影响的综合模型，可为临床抑郁症和失眠共病的治疗方案提供新思路。.