调动活化（TAR）DNA结合蛋白43千道尔顿（TDP-43）包涵体在几种神经退行性疾病中频繁发生，包括阿尔茨海默病、亨廷顿病、刘易斯小体病和进行性核上性麻痹，也可能与非退行性神经病因，例如肿瘤性、寄生肿瘤性、创伤性或感染性疾病相关联。与TDP-43诱导的神经退行性相关的多种病理蛋白质和机制之间的关系仍未完全理解。因此，不同病理机制的重叠经常导致更大的脑萎缩和更严重的临床过程，这表明共发病是临终诊断和治疗中的重要因素。本综述的目的是讨论TDP-43病理在其他主要，标志性病理即被称为TDP-43二级蛋白病的背景下的发生率、形态和作用。前文（第一部分）侧重于常见的神经退行性疾病，包括阿尔茨海默病、亨廷顿病和刘易斯小体病，而本文（第二部分）讨论了TDP-43病理与罕见的神经退行性疾病以及非退行性病因相关的神经疾病。

Transactivation (TAR) DNA binding protein 43 kDa (TDP-43) inclusions frequently occur as a comorbid pathology in several neurodegenerative disorders, including Alzheimer's disease, Huntington's disease, Lewy body disease, and progressive supranuclear palsy, and may appear in association with nondegenerative neurological etiology, for example neoplastic, paraneoplastic, traumatic, or infectious. Relationships between various pathological proteins and mechanisms associated with TDP-43-induced neurodegeneration are still not fully understood. Thus, overlap of distinct neuropathological mechanisms frequently leads to greater brain atrophy and a more severe clinical course, suggesting the importance of co-pathologies in ante-mortem diagnosing and treatment. The present review aims to discuss the incidence, morphology, and role of TDP-43 pathology in the context of other dominant, hallmark pathologies, referred to as secondary TDP-43 proteinopathies. The previous part (Part 1) focused on common neurodegenerative diseases, including Alzheimer's disease, Huntington's disease, and Lewy body disease, while the present part (Part 2) discusses TDP-43 pathology in rare neurodegenerative diseases and neurological diseases with nondegenerative etiology.