Bidirectional mechanism of comorbidity of depression and insomnia based on synaptic plasticity
10.11817/j.issn.1672-7347.2023.230082
- VernacularTitle:从突触可塑性出发探讨抑郁症和失眠的共病双向机制
- Author:
Fanhao MENG
1
;
Long WANG
Author Information
1. 黑龙江中医药大学第一临床医学院,哈尔滨 150040
- Keywords:
depression;
insomnia;
synaptic plasticity;
gene;
immune inflammation;
hypothalamic-pituitary-adrenal;
brain reward mechanism
- From:
Journal of Central South University(Medical Sciences)
2023;48(10):1518-1528
- CountryChina
- Language:Chinese
-
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.
