Kondo Reon, Mori Daisuke, Wake Hiroaki, Ozaki Norio
Department of Psychiatry, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Department of Anatomy and Molecular Cell Biology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Nagoya J Med Sci. 2025 May;87(2):196-210. doi: 10.18999/nagjms.87.2.196.
Mental disorders are a major global cause of disability that involve significant disturbances in thinking, emotional regulation, or behavior. The pathogenesis of these illnesses is complicated by their obscure nature and lack of biological markers. A genetics-first approach has been proposed to address this complexity. This approach associates clinical phenotypes with disease-susceptible genomic variants, such as copy number variations and single nucleotide variants. These rare variants significantly affect disease development and are thus crucial for assessing the effects of specific variants on disease and in determining the underlying biological mechanisms. In particular, mouse models that reflect these variants are instrumental in defining the causal relationships between genetic variants and disease-relevant phenotypes. Recent studies have highlighted the importance of sensory information processing in humans and mice. Advanced technologies that are valuable in unraveling the neural circuit mechanisms of these phenotypes include optogenetics and in vivo 2-photon imaging. Furthermore, mouse models can guide the integration of findings from patients and induced pluripotent stem cells, supporting a multidimensional approach to understanding the pathophysiology of mental disorders. In this review, we briefly discuss the utility of mouse models in a genetics-first approach to elucidate the pathophysiology of mental disorders. We also present examples of our mouse models based on rare disease-susceptible variants.
精神障碍是全球残疾的主要原因,涉及思维、情绪调节或行为的显著紊乱。这些疾病的发病机制因其性质模糊和缺乏生物标志物而变得复杂。有人提出了一种以遗传学为先的方法来应对这种复杂性。这种方法将临床表型与疾病易感性基因组变异联系起来,如拷贝数变异和单核苷酸变异。这些罕见变异显著影响疾病发展,因此对于评估特定变异对疾病的影响以及确定潜在的生物学机制至关重要。特别是,反映这些变异的小鼠模型有助于确定遗传变异与疾病相关表型之间的因果关系。最近的研究强调了人类和小鼠中感觉信息处理的重要性。在揭示这些表型的神经回路机制方面有价值的先进技术包括光遗传学和体内双光子成像。此外,小鼠模型可以指导整合来自患者和诱导多能干细胞的研究结果,支持采用多维度方法来理解精神障碍的病理生理学。在这篇综述中,我们简要讨论了小鼠模型在以遗传学为先的方法中阐明精神障碍病理生理学的效用。我们还展示了基于罕见疾病易感性变异的小鼠模型实例。