A new perspective on Alzheimer's disease: m6A modification

As a neurodegenerative disease, Alzheimer's disease (AD) is characterized by synaptic loss, extracellular plaques of amyloid accumulation, hyperphosphorylation of tau, and neuroinflammation. Various biological processes are affected by epitranscriptomic modifications, which regulate the metabolism of mRNA in cells and regulate the expression of genes. In response to changes in m6A modification levels, the nervous system becomes dysfunctional and plays a significant role in the development of Alzheimer's disease. As a result of recent research, this paper reviews advances in the understanding of the regulatory mechanisms of m6A modification in the occurrence and development of AD. In addition, the article discusses recent research techniques related to animal models of m6A and AD. Furthermore, it discusses the possibility of studying the pathogenesis of AD at the level of the epitranscriptome, identifying early diagnostic markers, and screening for effective treatment options.

Automated summary

As a neurodegenerative disease, Alzheimer's disease (AD) is characterized by synaptic loss, extracellular plaques of amyloid accumulation, hyperphosphorylation of tau, and neuroinflammation. Epitranscriptomic modifications, such as m6A modification, play a significant role in the development of AD. This paper reviews the advances in understanding the regulatory mechanisms of m6A modification in the occurrence and development of AD, and discusses the research techniques related to animal models of m6A and AD, as well as the potential of studying the pathogenesis of AD at the level of the epitranscriptome and identifying early diagnostic markers and effective treatment options.