Exposure to stressful life events is associated with a high risk of developing psychiatric disorders with a wide variety of symptoms. Cognitive symptoms in stress-related psychiatric disorders can be particularly challenging to understand, both for those experiencing them and for health care providers. To gain insights, it is important to capture stress-induced structural, epigenomic, transcriptomic, and proteomic changes in relevant brain regions such as the amygdala, hippocampus, locus coeruleus, and prefrontal cortex that result in long-lasting alterations in brain function. In this review, we will emphasize a subset of stress molecular mechanisms that alter neuroplasticity, neurogenesis, and balance between excitatory and inhibitory neurons. Then, we discuss how to identify genetic risk factors that may accelerate stress-driven or stress-induced cognitive impairment. Despite the development of new technologies such as single-cell resolution sequencing, our understanding of the molecular effects of stress in the brain remains to be deepened. A better understanding of the diversity of stress effects in different brain regions and cell types is a prerequisite to open new avenues for mechanism-informed prevention and treatment of stress-related cognitive symptoms.

中文翻译：

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与认知相互作用的应力分子信号传导


暴露于压力性生活事件与患具有多种症状的精神疾病的高风险有关。压力相关精神疾病中的认知症状可能特别难以理解，无论是对于经历这些症状的人还是对于医疗保健提供者来说。为了获得洞察力，重要的是要捕捉压力诱导的相关大脑区域（如杏仁核、海马体、蓝斑和前额叶皮层）的结构、表观基因组、转录组和蛋白质组学变化，这些变化会导致大脑功能的长期改变。在这篇综述中，我们将强调改变神经可塑性、神经发生以及兴奋性和抑制性神经元之间平衡的应激分子机制的一个子集。然后，我们讨论了如何识别可能加速压力驱动或压力诱导的认知障碍的遗传风险因素。尽管单细胞分辨率测序等新技术不断发展，但我们对大脑中压力的分子效应的理解仍有待加深。更好地了解不同大脑区域和细胞类型中压力效应的多样性是为机制知情预防和治疗与压力相关的认知症状开辟新途径的先决条件。