Chong Zhao Zhong, Souayah Nizar
Department of Neurology, Rutgers University, New Jersey Medical School, Newark, NJ, USA.
Drug Discov Today. 2025 May;30(5):104351. doi: 10.1016/j.drudis.2025.104351. Epub 2025 Apr 4.
The aberrant expression of the transactive response DNA-binding protein of 43 kDa (TDP-43) has been closely associated with amyotrophic lateral sclerosis (ALS). Cytoplasmic inclusions containing TDP-43 can be found in the brain and spinal cord in up to 97% of ALS cases. Mutations in the TARDBP gene promote the nuclear export of TDP-43, increase cytoplasmic aggregation, and predispose TDP-43 to post-translational modifications. Cleavage of TDP-43 and the resulting C- and N-terminal fragments also contribute to the development of ALS. Cellularly, the resulting impairment of autophagy and mitochondria aggravates cellular damage and neurodegeneration. Given the contribution of pathogenic TDP-43 to the development of ALS, elucidating the mechanisms related to TDP-43 will facilitate finding therapeutic targets for the disease.
43 kDa反式激活应答DNA结合蛋白(TDP - 43)的异常表达与肌萎缩侧索硬化症(ALS)密切相关。在高达97%的ALS病例中,可在脑和脊髓中发现含有TDP - 43的细胞质内含物。TARDBP基因的突变促进TDP - 43的核输出,增加细胞质聚集,并使TDP - 43易于发生翻译后修饰。TDP - 43的切割以及由此产生的C末端和N末端片段也有助于ALS的发展。在细胞水平上,自噬和线粒体功能的受损会加剧细胞损伤和神经退行性变。鉴于致病性TDP - 43对ALS发展的作用,阐明与TDP - 43相关的机制将有助于找到该疾病的治疗靶点。