Fike John R, Rola Radoslaw, Limoli Charles L
Department of Neurological Surgery and Radiation Oncology, University of California, San Francisco, USA.
Neurosurg Clin N Am. 2007 Jan;18(1):115-27, x. doi: 10.1016/j.nec.2006.10.010.
Considerable data are now available regarding the radiation responsiveness of neural precursor cells that exist in the neurogenic regions of the mammalian forebrain. These cells and their progeny are extremely sensitive to irradiation, undergoing apoptosis after clinically relevant doses that do not result in overt tissue injury. In addition, there is compelling evidence that radiation significantly affects the whole process of neurogenesis and that the sensitivity depends, at least in part, on alterations in the microenvironment within which the precursor cells exist. Although provocative data exist suggesting that inflammation, oxidative stress, or morphologic relations influence neurogenesis, the precise mechanisms involved remain obscure and need to be investigated. Additionally, it is important to try to understand what these findings may mean in the context of radiation paradigms associated with the treatment of intracranial disease. Understanding how neural precursor cells respond to noxious stimuli is likely to lead to new therapeutic approaches that should restore neurogenesis and perhaps improve cognitive performance.
目前已有大量关于存在于哺乳动物前脑神经发生区域的神经前体细胞辐射反应性的数据。这些细胞及其后代对辐射极其敏感,在不导致明显组织损伤的临床相关剂量照射后会发生凋亡。此外,有令人信服的证据表明,辐射会显著影响神经发生的整个过程,并且敏感性至少部分取决于前体细胞所处微环境的改变。尽管存在一些引人关注的数据表明炎症、氧化应激或形态学关系会影响神经发生,但其中涉及的精确机制仍不清楚,需要进行研究。此外,重要的是要尝试理解这些发现在与颅内疾病治疗相关的辐射模式背景下可能意味着什么。了解神经前体细胞如何对有害刺激作出反应,可能会带来新的治疗方法,有望恢复神经发生并可能改善认知功能。