核酸(脱)甲基化与内源甲醛及认知损伤

核酸(DNA和RNA)甲基化/脱甲基是表观遗传调控的重要机制.甲醛参与DNA、RNA的甲基化/脱甲基过程,从而影响表观遗传的调节,包括学习记忆等认知功能.然而,甲醛代谢失调将影响核酸的甲基化与脱甲基,使动物的学习记忆能力下降,造成认知损伤.对北京地区604名老人(≥60岁)的调查显示,内源甲醛含量与被试受教育的年限相关,受教育程度越高,内源甲醛含量越低,反之亦然.这些结果表明,内源甲醛在人类学习记忆中扮演重要的角色,"活到老,学到老"可以延缓甲醛代谢失调引起的老年认知损伤.因此,研究内源甲醛代谢与核酸甲基化修饰之间的关系,对探索记忆储存及认知损伤等表观遗传学相关疾病的发生发展机制,具有一定的启示.

Nucleic Acid Methylation/demethylation, Endogenous Formaldehyde and Age-related Cognitive Impairment

Methylation/demethylation of DNA, RNA and histone plays important roles in epigenetic functions. Formaldehyde is a significant factor participating in reversible and dynamic methylation of the biomacromolecules. As recently reported, memory formation and cognitive dysfunction are correlated with endogenous formaldehyde metabolism. Imbalance of formaldehyde metabolism affects DNA/RNA methylation and demethylation. Concentrations of endogenous formaldehyde are positively correlated with the severity of cognitive impairment of Alzheimer's patients in clinics. As an epidemiological survey shows, the levels of endogenous formaldehyde in elderly humans are negatively correlated with education years, suggesting that formaldehyde acts like a key factor in human learning and memory. "Live and learn" may mitigate the progression of age-related cognitive impairment resulted from imbalance of formaldehyde metabolism. Further investigation of endogenous formaldehyde involved in epigenetic modificaion and regulation should be carried out to understand the pathomechanism of cognition and cognitive impairment.