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降低乙化对大脑损伤具有神经保护作用

Min-Kyoo Shin¹, Edwin Vázquez-Rosa¹, Yeojung Koh¹

¹Harrington Discovery Institute, University Hospitals Cleveland Medical Center, Cleveland, OH, USA; Department of Psychiatry, Case Western Reserve University, Cleveland, OH, USA; Geriatric Psychiatry, GRECC, Louis Stokes Cleveland VA Medical Center; Cleveland, OH, USA; Institute for Transformative Molecular Medicine, School of Medicine, Case Western Reserve University, Cleveland, OH, USA.

|April 14, 2021

概括

创伤性脑损伤 (TBI) 触发了乙化,这是阿尔茨海默病 (AD) 的关键标志物. 针对这一过程可以预防TBI诱导的神经退行,并作为诊断生物标志物.

科学领域:

神经科学
生物化学
病理学

背景情况:

创伤性脑损伤 (TBI) 是阿尔茨海默病 (AD) 的重要危险因素.
这可能是神经退行性疾病的标志.
关联TBI与AD类病理的特定分子途径需要阐明.

研究的目的:

调查TBI诱导乙化的分子机制.
确定TBI诱导的乙烯化是否是一种潜在的治疗标.
探索TBI,乙烯和阿尔茨海默病进展之间的联系.

主要方法:

使用TBI的小鼠模型来检查tau乙化.
研究S-nitrosylated-GAPDH,Sirtuin1和p300/CBP在TBI诱导的乙烯化中的作用.
评估神经行为结果和测量大脑和血液中的ac-tau水平.

主要成果:

在人类AD大脑中发现的部位诱导tau乙化 (ac-tau).
通过非激活Sirtuin1和激活p300/ CBP,增加神经元活动,S- 基化- GAPDH调解了这一过程.
针对GAPDHS-化,p300/CBP或Sirtuin1的干预措施可以防止TBI诱导的神经退行和ac-tau积累.
发现AC-tau在TBI后的血液中积累.
在有TBI病史的患者中,AD大脑中的ac- tau增加进一步升高.

结论:

在阿尔茨海默病病理学中,TBI诱导了一种特定的乙烯化形式.
作为TBI的潜在治疗标和血液生物标志物,
药理上抑制p300/ CBP与AD和TBI的发病率降低有关.
这项研究突出了TBI和AD之间的潜在病理趋同.

关键词:

阿尔茨海默病 P7C3 其他乙化生产肌肉发育不良不同类型神经退行症神经保护其他药物盐酸盐没有.创伤性脑损伤

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