The aging central nervous system (CNS) of mammals displays progressive limited regenerative abilities. Recovery after loss of neurons is extremely restricted in the aged brain. Many research models fall short in recapitulating mammalian aging hallmarks or have an impractically long lifespan. We established a traumatic brain injury model in the African turquoise killifish (Nothobranchius furzeri), a regeneration-competent vertebrate that evolved to naturally age extremely fast. Stab-wound injury of the aged killifish dorsal telencephalon unveils an impaired and incomplete regeneration response when compared to young individuals. In the young adult killifish, brain regeneration is mainly supported by atypical non-glial progenitors, yet their proliferation capacity clearly declines with age. We identified a high inflammatory response and glial scarring to also underlie the hampered generation of new neurons in aged fish. These primary results will pave the way to unravel the factor age in relation to neurorepair, and to improve therapeutic strategies to restore the injured and/or diseased aged mammalian CNS.

中文翻译：

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衰老会损害非胶质祖细胞对鳉鱼 Nothobranchius furzeri 背侧端脑神经修复的重要贡献

哺乳动物老化的中枢神经系统 (CNS) 显示出逐渐受限的再生能力。在衰老的大脑中，神经元丢失后的恢复受到极大限制。许多研究模型无法概括哺乳动物的衰老特征，或者寿命长得不切实际。我们在非洲绿松石鳉鱼（ Nothobranchius furzeri）中建立了脑外伤模型)，一种具有再生能力的脊椎动物，进化到自然衰老的速度极快。与年轻人相比，老年鳉鱼背侧端脑的刺伤揭示了受损和不完整的再生反应。在年轻的成年鳉鱼中，脑再生主要由非典型非胶质祖细胞支持，但它们的增殖能力随着年龄的增长而明显下降。我们确定了高炎症反应和胶质瘢痕形成也是老年鱼新神经元生成受阻的基础。这些初步结果将为揭示与神经修复相关的因素年龄铺平道路，并改进治疗策略以恢复受伤和/或患病的老年哺乳动物中枢神经系统。