Abstract
ATP-binding cassette transporter A7 (ABCA7) is expressed in the hippocampus and cortex of the brain and was confirmed to be involved in the development of Alzheimer's disease (AD). Previous studies have demonstrated that ABCA7 regulated Aβ production, lipid transport, leading to AD characteristic pathological changes. However, the role and mechanism of ABCA7 in the context of AD needs further research. We augmented the expression of ABCA7 using lentiviral vector carrying ABCA7 gene to investigate the effect of ABCA7 overexpression on AD mice; then, we further explored the underlying mechanism in vitro. In the present study, ABCA7 was expressed successfully in the hippocampus of AD mice through lentiviral vector mediating ABCA7 gene; we showed that ABCA7 overexpression can effectively improve cognitive behavior of AD mice and diminished Aβ production; meanwhile, ABCA7 overexpression significantly relieved the neurotoxicity of Aβ by promoting cell viability and reducing endoplasmic reticulum stress. In conclusion, our findings showed that ABCA7 had obvious anti-Aβ effect and appeared to improve cognitive function of AD mice. Our results provided a new thought and basic scientific data for the clinical treatment of AD.
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