期刊
JOURNAL OF ALZHEIMERS DISEASE
卷 80, 期 3, 页码 1311-1327出版社
IOS PRESS
DOI: 10.3233/JAD-201162
关键词
APOE; CLU; morphometry; subcortical structures; synergistic
资金
- National Key Research and Development Program of China [2019YFA0706200]
- National Natural Science Foundation of China [61632014, 61627808, 61210010]
- National Basic Research Program of China (973 Program) [2014CB744600]
- Gansu Science and Technology Program [17JR7WA026]
- Program of Beijing Municipal Science & Technology Commission [Z171100000117005]
- Natural Science Foundation of Gansu Province of China [20JR5RA292]
- Fundamental Research Funds for the Central Universities [lzujbky-2018-it67, lzujbky-2018-it64, lzuxxxy-2018-it70]
The study revealed synergistic effects of APOE and CLU genes on the morphological degeneration of the hippocampus and amygdala in non-demented elderly individuals, suggesting a complex interaction between genetic variants in understanding the pathogenesis of Alzheimer's disease.
Background: The volume loss of the hippocampus and amygdala in non-demented individuals has been reported to increase the risk of developing Alzheimer's disease (AD). Many neuroimaging genetics studies mainly focused on the individual effects of APOE and CLU on neuroimaging to understand their neural mechanisms, whereas their synergistic effects have been rarely studied. Objective: To assess whether APOE and CLU have synergetic effects, we investigated the epistatic interaction and combined effects of the two genetic variants on morphological degeneration of hippocampus and amygdala in the non-demented elderly at baseline and 2-year follow-up. Methods: Besides the widely-used volume indicator, the surface-based morphometry method was also adopted in this study to evaluate shape alterations. Results: Our results showed a synergistic effect of homozygosity for the CLU risk allele C in rs11136000 and APOE epsilon 4 on the hippocampal and amygdalar volumes during a 2-year follow-up. Moreover, the combined effects of APOE epsilon 4 and CLU C were stronger than either of the individual effects in the atrophy progress of the amygdala. Conclusion: These findings indicate that brain morphological changes are caused by more than one gene variant, which may help us to better understand the complex endogenous mechanism of AD.
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