Department of Pathology, Boston Children's Hospital, Boston, MA 02115, USA.
Department of Pathology, Boston Children's Hospital, Boston, MA 02115, USA; Graduate Program in Biological and Biomedical Sciences, Harvard Medical School, Boston, MA 02115, USA; Harvard, MIT MD-PhD Program, Harvard Medical School, Boston, MA 02115, USA.
Neuron. 2022 Oct 19;110(20):3288-3301.e8. doi: 10.1016/j.neuron.2022.08.009. Epub 2022 Sep 6.
For many cancer patients, chemotherapy produces untreatable life-long neurologic effects termed chemotherapy-related cognitive impairment (CRCI). We discovered that the chemotherapy methotrexate (MTX) adversely affects oxidative metabolism of non-cancerous choroid plexus (ChP) cells and the cerebrospinal fluid (CSF). We used a ChP-targeted adeno-associated viral (AAV) vector approach in mice to augment CSF levels of the secreted antioxidant SOD3. AAV-SOD3 gene therapy increased oxidative defense capacity of the CSF and prevented MTX-induced lipid peroxidation in the hippocampus. Furthermore, this gene therapy prevented anxiety and deficits in short-term learning and memory caused by MTX. MTX-induced oxidative damage to cultured human cortical neurons and analyses of CSF samples from MTX-treated lymphoma patients demonstrated that MTX diminishes antioxidant capacity of patient CSF. Collectively, our findings motivate the advancement of ChP- and CSF-targeted anti-oxidative prophylactic measures to relieve CRCI.
对于许多癌症患者来说,化疗会产生无法治疗的终身神经学影响,称为化疗相关性认知障碍(CRCI)。我们发现,化疗药物甲氨蝶呤(MTX)会对非癌性脉络丛(ChP)细胞和脑脊液(CSF)的氧化代谢产生不利影响。我们使用针对 ChP 的腺相关病毒(AAV)载体方法在小鼠中增加 CSF 中分泌的抗氧化剂 SOD3 的水平。AAV-SOD3 基因治疗增加了 CSF 的氧化防御能力,并防止了 MTX 诱导的海马体中的脂质过氧化。此外,这种基因治疗还可以预防 MTX 引起的焦虑和短期学习记忆障碍。MTX 对培养的人皮质神经元的氧化损伤以及对接受 MTX 治疗的淋巴瘤患者的 CSF 样本的分析表明,MTX 降低了患者 CSF 的抗氧化能力。总的来说,我们的发现促使人们采取针对 ChP 和 CSF 的抗氧化预防措施来缓解 CRCI。