Institute of Clinical Neurobiology, Alberichgasse 5/13, 1150, Vienna, Austria.
J Neural Transm (Vienna). 2024 Feb;131(2):107-115. doi: 10.1007/s00702-023-02714-6. Epub 2023 Nov 3.
Depression with an average prevalence of 25-40% is a serious condition in amyotrophic lateral sclerosis (ALS) that can impact quality of life and survival of patients and caregiver burden, yet the underlying neurobiology is poorly understood. Preexisting depression has been associated with a higher risk of developing ALS, while people with ALS have a significantly higher risk of developing depression that can cause multiple complications. Depression may be a prodromal or subclinical symptom prior to motor involvement, although its relations with disease progression and impairment of quality of life are under discussion. Unfortunately, there are no studies existing that explore the pathogenic mechanisms of depression associated with the basic neurodegenerative process, and no specific neuroimaging data or postmortem findings for the combination of ALS and depression are currently available. Experience from other neurodegenerative processes suggests that depressive symptoms in ALS may be the consequence of cortical thinning in prefrontal regions and other cortex areas, disruption of mood-related brain networks, dysfunction of neurotransmitter systems, changing cortisol levels and other, hitherto unknown mechanisms. Treatment of both ALS and depression is a multidisciplinary task, depression generally being treated with a combination of antidepressant medication, physiotherapy, psychological and other interventions, while electroconvulsive therapy and deep brain stimulation might not be indicated in the majority of patients in view of their poor prognosis. Since compared to depression in other neurodegenerative diseases, our knowledge of its molecular basis in ALS is missing, multidisciplinary clinicopathological studies to elucidate the pathomechanism of depression in motor system disorders including ALS are urgently warranted.
抑郁症在肌萎缩侧索硬化症(ALS)中的平均患病率为 25-40%,是一种严重的疾病,会影响患者的生活质量和生存以及照顾者的负担,但潜在的神经生物学机制仍不清楚。先前存在的抑郁症与发生 ALS 的风险增加有关,而 ALS 患者发生抑郁症的风险明显更高,这可能导致多种并发症。抑郁症可能是运动障碍之前的前驱或亚临床症状,尽管其与疾病进展和生活质量受损的关系仍在讨论中。不幸的是,目前尚无研究探讨与基本神经退行性过程相关的抑郁症的发病机制,也没有针对 ALS 和抑郁症结合的特定神经影像学数据或尸检结果。来自其他神经退行性过程的经验表明,ALS 中的抑郁症状可能是前额叶区域和其他皮质区域皮质变薄、情绪相关脑网络中断、神经递质系统功能障碍、皮质醇水平变化和其他迄今未知机制的后果。ALS 和抑郁症的治疗都是多学科的任务,抑郁症通常采用抗抑郁药物、物理治疗、心理和其他干预措施的组合进行治疗,而鉴于大多数患者预后较差,电惊厥疗法和深部脑刺激可能不适用于大多数患者。由于与其他神经退行性疾病中的抑郁症相比,我们对 ALS 中其分子基础的了解还存在不足,因此迫切需要进行多学科临床病理研究,以阐明包括 ALS 在内的运动系统疾病中抑郁症的发病机制。