长期以来,科学家认为一种特殊的DNA损伤--DNA双链断裂(DSB)对脑细胞特别有害,是老年病如老年痴呆背后的主要推手。据物理学家组织网3月24日报道,最近,美国加利福尼亚大学旧金山分校格拉斯通研究所科学家发现,DSB实际上是一种常规的、非伤害性脑活动过程的一部分。这一发现有助于理解老年痴呆症背后的机制。他们还利用小鼠模型确定了两种治疗方案,能降低老年痴呆症中过高的DSB破坏。相关论文发表在24日的《自然-神经科学》(Nature Neuroscience)上。该论文指出,只要DSB是在严格控制之下并能及时修复,神经元中的DSB也是正常脑功能(如学习功能)的一部分。脑中淀粉样β蛋白积 For a long time, scientists have identified a particular type of DNA damage - DNA double-strand breaks (DSBs) that are particularly detrimental to brain cells and are the prime mover behind geriatric diseases such as dementia. According to the March 24 report of the Physicist’s Organization, recently, scientists at the Glaston Research Institute at the University of California, San Francisco, found that DSB is actually part of a routine, non-nociceptive brain activity process. This finding helps to understand the mechanisms behind dementia. They also used the mouse model to identify two treatment options that reduce excessive DSB damage in Alzheimer’s disease. Relevant papers published in the 24th of “Nature - Neuroscience” (NatureNeuroscience). The paper states that DSBs in neurons are also part of normal brain functions (such as learning function) as long as DSBs are under strict control and can be repaired promptly. Brain amyloid beta protein product