神经退行性疾病具有复杂的起源，由遗传和环境因素组成。 DNA 损伤和染色质重排都是在病理条件下和正常功能的神经元中发生的重要过程。虽然大量研究已经证明 DNA 损伤和染色质组织之间存在不可分割的关系，但对这种关系的理解，尤其是在神经退行性疾病中，还需要进一步研究。有趣的是，最近的研究表明，参与神经退行性疾病的已知标志蛋白在 DNA 损伤和染色质重组中发挥作用，这篇综述讨论了目前对这种关系的认识。本综述重点关注各种神经退行性疾病中涉及的标志蛋白，例如微管相关蛋白 tau、TAR DNA/RNA 结合蛋白 43 (TDP-43)、超氧化物歧化酶 1 (SOD1)、肉瘤融合蛋白 (FUS)、亨廷顿蛋白 (FUS)。 HTT)、α-突触核蛋白和 β-淀粉样前体蛋白 (APP)。因此，DNA 损伤和染色质重排与不同神经退行性疾病的疾病机制相关。针对 DNA 修复和染色质重组的常见调节剂可能会带来治疗神经退行性病变的有前途的疗法。© 2024。作者。

Neurodegenerative diseases have a complex origin and are composed of genetic and environmental factors. Both DNA damage and chromatin rearrangement are important processes that occur under pathological conditions and in neurons functioning properly. While numerous studies have demonstrated the inseparable relationship between DNA damage and chromatin organization, understanding of this relationship, especially in neurodegenerative diseases, requires further study. Interestingly, recent studies revealed that known hallmark proteins involved in neurodegenerative diseases function in both DNA damage and chromatin reorganization, and this review discusses the current knowledge of this relationship. This review focused on hallmark proteins involved in various neurodegenerative diseases, such as the microtubule-associated protein tau, TAR DNA/RNA binding protein 43 (TDP-43), superoxide dismutase 1 (SOD1), fused in sarcoma (FUS), huntingtin (HTT), α-synuclein, and β-amyloid precursor protein (APP). Hence, DNA damage and chromatin rearrangement are associated with disease mechanisms in distinct neurodegenerative diseases. Targeting common modulators of DNA repair and chromatin reorganization may lead to promising therapies for treating neurodegeneration.© 2024. The Author(s).