Mou Ya-Kui, Guan Li-Na, Yao Xiao-Yan, Wang Jia-Hui, Song Xiao-Yu, Ji Yong-Qiang, Ren Chao, Wei Shi-Zhuang
Department of Otolaryngology, Head and Neck Surgery, Yantai Yuhuangding Hospital, Qingdao University, Yantai, China.
Department of Neurosurgical Intensive Care Unit, Yantai Yuhuangding Hospital, Qingdao University, Yantai, China.
Front Aging Neurosci. 2022 May 13;14:890512. doi: 10.3389/fnagi.2022.890512. eCollection 2022.
Depression can be a non-motor symptom, a risk factor, and even a co-morbidity of Parkinson's disease (PD). In either case, depression seriously affects the quality of life of PD patients. Unfortunately, at present, a large number of clinical and basic studies focused on the pathophysiological mechanism of PD and the prevention and treatment of motor symptoms. Although there has been increasing attention to PD-related depression, it is difficult to achieve early detection and early intervention, because the clinical guidelines mostly refer to depression developed after or accompanied by motor impairments. Why is there such a dilemma? This is because there has been no suitable preclinical animal model for studying the relationship between depression and PD, and the assessment of depressive behavior in PD preclinical models is as well a very challenging task since it is not free from the confounding from the motor impairment. As a common method to simulate PD symptoms, neurotoxin-induced PD models have been widely used. Studies have found that neurotoxin-induced PD model animals could exhibit depression-like behaviors, which sometimes manifested earlier than motor impairments. Therefore, there have been attempts to establish the PD-related depression model by neurotoxin induction. However, due to a lack of unified protocol, the reported results were diverse. For the purpose of further promoting the improvement and optimization of the animal models and the study of PD-related depression, we reviewed the establishment and evaluation strategies of the current animal models of PD-related depression based on both the existing literature and our own research experience, and discussed the possible mechanism and interventions, in order to provide a reference for future research in this area.
抑郁症可能是帕金森病(PD)的非运动症状、危险因素,甚至是共病。在任何一种情况下,抑郁症都会严重影响PD患者的生活质量。不幸的是,目前大量的临床和基础研究集中在PD的病理生理机制以及运动症状的防治上。尽管对PD相关性抑郁症的关注日益增加,但由于临床指南大多参考在运动障碍之后或伴随运动障碍出现的抑郁症,因此难以实现早期检测和早期干预。为什么会出现这样的困境呢?这是因为一直没有合适的临床前动物模型来研究抑郁症与PD之间的关系,而且在PD临床前模型中评估抑郁行为也是一项非常具有挑战性的任务,因为它无法摆脱运动障碍的混杂影响。作为模拟PD症状的常用方法,神经毒素诱导的PD模型已被广泛应用。研究发现,神经毒素诱导的PD模型动物可表现出类似抑郁的行为,有时这种行为比运动障碍出现得更早。因此,有人尝试通过神经毒素诱导建立PD相关性抑郁症模型。然而,由于缺乏统一的方案,报道的结果各不相同。为了进一步推动动物模型的改进和优化以及对PD相关性抑郁症的研究,我们基于现有文献和自身研究经验,综述了当前PD相关性抑郁症动物模型的建立和评估策略,并探讨了可能的机制和干预措施,以便为该领域的未来研究提供参考。