A link between DNA dna and Alzheimer's disease

Alzheimer's disease (AD) is a multi-factor disease closely related to aging, and its pathogenesis is more complex. The main neuropathological features of AD are β-amyloid protein deposition to form plaques and micro-tube protein tau excessive phosphate to form nerve fiber entanglements. Previous studies of brain tissue samples and model mice in AD patients have found significant apparent regulatory changes and dysfunctions, including DNA methylation and de-methylation, during degenerative lesions of AD neurons. As an important surface control system of the body, DNA methylation and dna methylation are involved in many biological processes and are closely related to the development of many diseases. But academics don't yet know "what are the characteristics of DNA methylation and demethylation abnormal changes that occur in AD neuron degenerative lesions?". Does it involve and affect degenerative lesions of AD neurons? "and so on."
To this end, Li Jiali, a researcher at the
Kunming Institute of Zoology in Kunming, China, used brain tissue samples from AD patients and mice with 3xTg AD models to detect and analyze the dynamic changes in DNA demethylation in AD neuron degenerative lesions, and to study in depth the possible role and structure in AD neuron degenerative lesions. Hydroxy-methyl cytosine (5hmC) is an important intermediate product of DNA de-methylation, and its mediated surface regulation involves more biological processes. The study found significant loss of 5hmC levels in the cerebral cortical layer and hippocupal regions in AD patients and 3xTg AD mice. Point hybridization and hMeDIP-seq results showed that in AD mice, the overall level of neuron 5hmC showed a more significant decrease than that of glial cells, and bioinsynistics showed that the loss of 5hmC was closely related to the expression disorder of genes associated with neuron survival and synth plasticity. Current studies suggest that the process of converting 5-methyl cytosine (5mC) into 5hmC is mainly catalyticly regulated by the TET enzyme family. The researchers found significantly lower levels of TAT enzymes in the cerebral cortical and hippocupal regions of AD patients and model mice, suggesting that this may have been a significant cause of the lower 5hmC levels. To clarify the role of different subtypes of TAT enzymes in AD, the researchers expressed the enzyme activity regions of TAT enzyme families 3 members in the sea mass of AD mice and found that the active regions of TAT3 enzymes were effective in improving neuron degenerative lesions in mice, including reducing A-beta deposition, geriatric plaque formation and tau protein excessive phosphocysis and neurofibromatic tangle formation; The study reveals the important role of 5hmC-mediated metastrative disorders in the process of AD neuron degenerative lesions, and is conducive to an in-depth understanding of the biological role of abnormal changes in DNA methylation and de-methylation in aging-related neurodegenerative diseases.
recently, the results of the study were published online in THE FASEB Journal. Li Jiali is the co-author of the thesis, Zhang Ying, Ph.D. graduate student of Kunming Animal Institute, Zhang Zhongyu, Ph.D. student of Peking University, Li Lianwei and Xu Kaiyu, ph.D. student of Kunming Zo institute. The research was supported by Zhou Xiwen, an assistant professor at
Chinese University, Herrup Karl, a professor at the University of Pittsburgh in the United States, Liu Quanping, a professor at Huahua University of Science and Technology, and Ma Zhanshan, a researcher at kunming Animal Institute, and was supported by the National Natural Science Foundation of China and the Ministry of Science and Technology's key research and development programs. (Source: Kunming Zoological Research Institute)
related paper information:Kunming animals revealed a link between DNA dna and Alzheimer's disease