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<p>During human evolution, some genes were lost or silenced from the genome of hominins. These missing genes might be the key to the evolution of humans’ unique cognitive skills. An inactivation mutation in CMP-<i>N</i>-acetylneuraminic acid hydroxylase (<i>CMAH</i>) was the result of natural selection. The inactivation of <i>CMAH</i> protected our ancestors from some pathogens and reduced the level of <i>N</i>-glycolylneuraminic acid (Neu5Gc) in brain tissue. Interestingly, the low level of Neu5Gc promoted the development of brain tissue, which may have played a role in human evolution. As a xenoantigen, Neu5Gc may have been involved in brain evolution by affecting neural conduction, neuronal development, and aging.</p> Graphical Abstract <p>During human evolution, humans lost the ability to synthesize Neu5Gc after the inactivation mutation of the gene <i>CMAH</i>. Therefore, Neu5Gc in the human body is a xenoantigen. The inactivation of <i>CMAH</i> and the loss of endogenous Neu5Gc may have played a role in human brain evolution by affecting neural conduction, neuronal development, and aging.</p> <p></p>

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Inactivation of the CMAH gene and deficiency of Neu5Gc play a role in human brain evolution

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年2月8日

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  • Yuxin Liu,
  • Jinhong Li,
  • Qicai Liu

摘要

During human evolution, some genes were lost or silenced from the genome of hominins. These missing genes might be the key to the evolution of humans’ unique cognitive skills. An inactivation mutation in CMP-N-acetylneuraminic acid hydroxylase (CMAH) was the result of natural selection. The inactivation of CMAH protected our ancestors from some pathogens and reduced the level of N-glycolylneuraminic acid (Neu5Gc) in brain tissue. Interestingly, the low level of Neu5Gc promoted the development of brain tissue, which may have played a role in human evolution. As a xenoantigen, Neu5Gc may have been involved in brain evolution by affecting neural conduction, neuronal development, and aging.

Graphical Abstract

During human evolution, humans lost the ability to synthesize Neu5Gc after the inactivation mutation of the gene CMAH. Therefore, Neu5Gc in the human body is a xenoantigen. The inactivation of CMAH and the loss of endogenous Neu5Gc may have played a role in human brain evolution by affecting neural conduction, neuronal development, and aging.