改变的素乙化与老年依赖性记忆障碍在小鼠中有关
Shahaf Peleg1, Farahnaz Sananbenesi, Athanasios Zovoilis
1Laboratory for Aging and Cognitive Diseases, European Neuroscience Institute, Grisebach Str. 5, D-37077 Goettingen, Germany.
Science (New York, N.Y.)
|May 8, 2010
概括
在老鼠中,与年龄相关的记忆障碍与基因素乙化变化有关. 恢复素H4 lysine 12乙化恢复了认知功能,这表明大脑衰老的潜在生物标志物.
科学领域:
- 神经科学是一个神经科学.
- 表观遗传学 在表观遗传学中,表观遗传学是指表观遗传学.
- 衰老研究研究 衰老研究
背景情况:
- 认知能力下降是一个越来越令人担忧的人类寿命的增加.
- 与年龄相关的记忆障碍的机制在很大程度上是未知的.
- 老化的大脑经历了影响认知的分子通路的显著变化.
研究的目的:
- 为了研究衰老大脑中潜在的记忆障碍的分子机制.
- 为了确定潜在的生物标志物对认知衰退的衰老.
- 探索染色质可塑性在与年龄相关的记忆障碍中的作用.
主要方法:
- 在老年小鼠中研究记忆功能和海马色素可塑性.
- 在学习过程中分析 histone H4 lysine 12 (H4K12) 乙化模式.
- 评估与记忆巩固相关的基因表达程序.
- 进行干预以恢复H4K12乙化水平.
主要成果:
- 年龄较大的小鼠在学习过程中表现出海马色素可塑性的改变和H4K12乙化失调.
- 在老年小鼠中观察到未能启动海马体基因表达程序.
- 恢复H4K12乙化使基因表达正常化并恢复认知能力.
结论:
- 不调节的H4K12乙化与老化老鼠大脑中的记忆缺陷有关.
- 恢复H4K12乙化可以逆转与年龄相关的认知衰退.
- 改变的H4K12乙化可能成为衰老大脑中受损的基因组环境相互作用的早期生物标志物.
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