Neurodegenerative diseases, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS), are characterized by the progressive loss of neuronal function and structure. While several genetic and environmental factors have been implicated in the pathogenesis of these disorders, emerging evidence suggests that transposable elements (TEs), once considered “junk DNA,” play a significant role in their development and progression. TEs are mobile genetic elements capable of moving within the genome, and their dysregulation has been associated with genomic instability, altered gene expression, and neuroinflammation. This review provides an overview of TEs, including long interspersed nuclear elements (LINEs), short interspersed nuclear elements (SINEs), and endogenous retroviruses (ERVs), mechanisms of repression and derepression, and their potential impact on neurodegeneration. The evidence linking TEs to AD, PD, and ALS by shedding light on the complex interactions between TEs and neurodegeneration has been discussed. Furthermore, the therapeutic potential of targeting TEs in neurodegenerative diseases has been explored. Understanding the role of TEs in neurodegeneration holds promise for developing novel therapeutic strategies aimed at mitigating disease progression and preserving neuronal health.

神经退行性疾病，如阿尔茨海默病 (AD)、帕金森病 (PD) 和肌萎缩侧索硬化症 (ALS)，其特征是神经元功能和结构的进行性丧失。虽然一些遗传和环境因素与这些疾病的发病机制有关，但新出现的证据表明，曾经被认为是“垃圾DNA”的转座元件（TE）在这些疾病的发生和进展中发挥着重要作用。TE 是能够在基因组内移动的可移动遗传元件，它们的失调与基因组不稳定、基因表达改变和神经炎症有关。本综述概述了 TE，包括长散布核元件 (LINE)、短散布核元件 (SINE) 和内源性逆转录病毒 (ERV)、抑制和去抑制机制及其对神经退行性变的潜在影响。通过阐明 TE 与神经退行性变之间复杂的相互作用，将 TE 与 AD、PD 和 ALS 联系起来的证据已经得到讨论。此外，针对神经退行性疾病中 TE 的治疗潜力也得到了探索。了解 TE 在神经退行性变中的作用有望开发旨在减缓疾病进展和保持神经元健康的新型治疗策略。