神经发育障碍中的大脑衰老:对氧化,炎症和线粒体机制的叙述性审查
Maiara de Aguiar da Costa1, Victória Linden de Rezende1, Sofia Januário Bolan1
1Departamento de Neurologia Experimental, Laboratório de Autismo e Neurodesenvolvimento, Universidade do Extremo Sul Catarinense, UNESC, Criciúma, Brazil.
Neurodegenerative disease management
|February 4, 2026
概括
患有神经发育障碍 (NDD) 的人可能会经历加速的大脑衰老,增加认知能力下降和神经退行性疾病的风险. 研究突出了共享的生物途径和生物标志物,表明NDDs的改变衰老轨迹.
科学领域:
- 神经科学是一个神经科学.
- 衰老研究研究 衰老研究
- 发展生物学 发展生物学
背景情况:
- 神经发育障碍 (NDD) 包括自闭症谱系障碍和唐氏综合征等疾病.
- 越来越多的证据表明,患有NDD的个体可能表现出不典型或加速的大脑衰老.
- 这种衰老模式与认知能力下降和对神经退行性疾病的脆弱性增加有关.
研究的目的:
- 审查目前关于推动NDDs改变衰老的生物机制的研究结果.
- 探索NDD和神经退行症之间的共同途径.
- 讨论生物标志物和环境因素在神经分化个体的衰老结果中的作用.
主要方法:
- 现有文献的叙述性审查.
- 对生物机制 (氧化应激,神经炎症,线粒体功能障碍,细胞衰老) 的综合研究.
- 对生物标记数据 (端粒长度,血GFAP/NfL,脑年龄成像) 和心理社会/环境因素的分析.
主要成果:
- 共有的分子通路,包括氧化应激和神经炎症,都与NDD和神经退行有关.
- 诸如端粒缩短,高GFAP/NfL和改变的大脑年龄等生物标志物支持NDD的加速衰老.
- 异质性,有限的纵向数据和心理社会因素使因果推断复杂化.
结论:
- 在NDD中改变了生物衰老,可能增加了对早期神经退行症的易感性.
- 整合生物,行为和环境标志物对于监测和干预至关重要.
- 早期干预是必要的,以促进神经分化群体中更健康的认知和功能衰老.
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