Laboratory of Neurogenetics, Department of Neurodegenerative Disorders , Mossakowski Medical Research Centre, Polish Academy of Sciences , 5 Pawinskiego Street , 02-106 Warsaw , Poland.
ACS Chem Neurosci. 2018 May 16;9(5):870-872. doi: 10.1021/acschemneuro.8b00149. Epub 2018 Apr 10.
Oxidative damage of DNA has recently been indicated as one of the strong pathogenic agent in Alzheimer's disease (AD). Oxidative stress induces numerous signaling pathways, including DNA damage response (DDR), associated with the breast cancer type 1 susceptibility protein (BRCA1) protein, known to date from numerous reports in the cancer field. In this Viewpoint, we discuss the latest discoveries related to the role of BRCA1 in the death of neurons in AD. We underline the role of BRCA1 in the development of neurons and speculate on the consequences of BRCA1 dysfunction in the dying brain. In general, this Viewpoint is in a line with several recent reports on the processes and players common at the molecular and genetic level for neurodegenerative and cancerous diseases.
DNA 的氧化损伤最近被认为是阿尔茨海默病 (AD) 的主要致病因素之一。氧化应激诱导了许多信号通路，包括与乳腺癌类型 1 易感性蛋白 (BRCA1) 相关的 DNA 损伤反应 (DDR)，这一蛋白在癌症领域的众多报告中已为人所知。在本观点中，我们讨论了与 BRCA1 在 AD 中神经元死亡中的作用相关的最新发现。我们强调了 BRCA1 在神经元发育中的作用，并推测 BRCA1 功能障碍对垂死大脑的后果。总的来说，本观点与最近关于分子和遗传水平上神经退行性疾病和癌症共同过程和参与者的几项报告一致。
