The study revealed the mechanism by which APOE4 regulates Alzheimer's disease

September 3rd, Professor Jia Jianping of Xuanwu Hospital, Capital Medical University, published a study online in the journal Alzheimer's disease and dementia on the distribution and action patterns of the Alzheimer's risk gene APOE 4. For the first time, the study analyzed the carrying condition of Chinese lipoprotein E4 (APOE) and finally confirmed the strong correlation between APOE 4 and Alzheimer's disease (AD), and revealed that the APOE 4 allied gene played a different risk effect in the three AD subtypes, especially in familial ADs with unknown gene mutations.
about 20% of the normal population in China carry the APOE 4 genotype, which is considered to be the main genetic risk factor. The findings of this study provide a theoretical basis for the establishment of large-scale population intervention. Jia Longfei, the first author of the paper and deputy director of Xuanwu Hospital at Capital Medical University, said.
it is understood that the study included a total of 15,119 subjects, including normal people, known gene mutations of familial AD, distributed AD, unknown gene mutations of familial AD, the frequency distribution of the APOE 4 genotype showed an increasing trend, respectively, 19.54 percent, 26.19 percent, 36.23 percent, 56.27 percent. According to the risk prediction model established by APOE 4, APOE 4 has no risk effect on familial AD of known gene mutations, and has the strongest risk prediction ability for familial AD of unknown gene mutations.
"This is the largest Chinese study to date on the frequency distribution of APOE in this cluster. Jia Jianping, author of the paper, said that the results of the study gradually solved the mystery of the regulation of APOE 4 on AD prevalence, had an important impact on the pathogenesis of APOE 4 in the Chinese group, and also provided new ideas for AD genetic intervention and gene therapy in Chinese people, and hopefully from the aspect of gene editing, reduce the expression of AD risk genes, and find a new breakthrough point for the eventual cure of AD. (Source: Zhang Siwei, China Science Journal)
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