休斯顿卫理公会的一项研究将有缺陷的TDP43蛋白质与DNA修复问题联系起来,导致ALS和痴呆症等疾病的脑细胞损伤。 A Houston Methodist study links faulty TDP43 protein to DNA repair issues, driving brain cell damage in diseases like ALS and dementia.

休斯顿卫理公会的一项研究表明,TDP43是一种与痴呆症和ALS挂钩的蛋白质,对于DNA脱节修复至关重要。 A Houston Methodist study reveals that TDP43, a protein tied to dementia and ALS, is crucial for DNA mismatch repair. 当机能失调时,它会导致基因组不稳定,导致神经衰竭和潜在的癌症。 When dysfunctional, it causes genomic instability, contributing to neurodegeneration and potentially cancer. 研究人员发现异常的TDP43水平触发了过度活跃的DNA修复,导致神经元损伤。 Researchers found abnormal TDP43 levels trigger overactive DNA repair, leading to neuron damage. 减少这种过度活动扭转了实验室模型中的一些损害,为神经退化和其他疾病提供了新的治疗途径。 Reducing this overactivity reversed some damage in lab models, suggesting new therapeutic avenues for neurodegenerative and other diseases. 这些研究结果发表在《核酸研究》中,突出了蛋白质功能、遗传稳定性和大脑健康之间的关键联系。 The findings, published in Nucleic Acids Research, highlight a key link between protein function, genetic stability, and brain health.