Depression is one of the most frequent neuropsychiatric symptoms in corticobasal degeneration (CBD), a rare, sporadic, and late-onset progressive neurodegenerative disorder of unknown etiology. It is clinically characterized by a levodopa-poorly responsible akinetic-rigid syndrome, apraxia, limb dystonia, cognitive, mood, behavioral, and language disorders. This 4-repeat (4R) tauopathy is morphologically featured by asymmetric frontoparietal atrophy, neuronal loss, and gliosis in cortex and subcortex including substantia nigra, ballooned/achromatic neurons with filamentous 4R tau aggregates in cortex and striatum, widespread thread-like structures, pathognomonic "astroglial plaques", "tufted astrocytes", and numerous "coiled bodies" (in astrocytes and oligodendroglia) in cerebral white matter. CBD is non-specific, as pathologically proven cases include several clinical phenotypes. Pubmed and Google Scholar were systematically analyzed until October 2023, with focus on the prevalence, clinical manifestation, neuroimaging data, and treatment options of depression in CBD. Its prevalence is about 30–40% which is more frequent than in most other atypical parkinsonian syndromes. Depression usually does not correlate with motor and other clinical parameters, suggesting different pathophysiological mechanisms. Asymmetric atrophy and hypometabolism of frontoparietal cortical areas are associated with disruption of fronto-subcortical circuits, nigrostriatal dopaminergic, and cholinergic deficiency. Since no specific neuroimaging, neuropathological, or biomarker studies of depression in CBD are available, its pathobiological mechanisms and pathogenesis are poorly understood. Antidepressive therapy may be useful, but is often poorly tolerated. Depression in CBD, like in other parkinsonian syndromes, may be related to multi-regional patterns of cerebral disturbances and complex pathogenic mechanisms that deserve further elucidation as a basis for early diagnosis and adequate treatment to improve the quality of life in this fatal disease.

抑郁症是皮质基底节变性 (CBD) 中最常见的神经精神症状之一，这是一种罕见、散发性、迟发性、病因不明的进行性神经退行性疾病。其临床特征为左旋多巴不良运动不能性强直综合征、失用症、肢体肌张力障碍、认知、情绪、行为和语言障碍。这种 4 次重复 (4R) tau 蛋白病的形态学特征为不对称额顶萎缩、神经元缺失、皮质和皮质下层（包括黑质）神经胶质增生、皮质和纹状体中具有丝状 4R tau 聚集的气球状/消色差神经元、广泛的线状结构、特征性的大脑白质中的“星形胶质细胞斑块”、“簇状星形胶质细胞”和大量“卷曲体”（星形胶质细胞和少突胶质细胞）。CBD 是非特异性的，因为病理证实的病例包括多种临床表型。Pubmed 和 Google Scholar 对 2023 年 10 月之前的抑郁症进行了系统分析，重点关注 CBD 抑郁症的患病率、临床表现、神经影像数据和治疗选择。其患病率约为 30-40%，比大多数其他非典型帕金森综合征更为常见。抑郁症通常与运动和其他临床参数无关，表明不同的病理生理机制。额顶皮质区域的不对称萎缩和代谢低下与额皮质下回路破坏、黑质纹状体多巴胺能和胆碱能缺乏有关。由于尚无针对 CBD 抑郁症的具体神经影像学、神经病理学或生物标志物研究，因此对其病理生物学机制和发病机制知之甚少。抗抑郁治疗可能有用，但通常耐受性较差。与其他帕金森综合征一样，CBD 中的抑郁症可能与多区域脑紊乱模式和复杂的致病机制有关，值得进一步阐明，作为早期诊断和充分治疗的基础，以提高这种致命疾病的生活质量。