ArticleJournal of molecular neuroscience : MN2017
Study on Lentivirus-Mediated ABCA7 Improves Neurocognitive Function and Related Mechanisms in the C57BL/6 Mouse Model of Alzheimer's Disease.
Article in Journal of molecular neuroscience : MN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- The role of ATP-binding cassette subfamily A in the etiology of Alzheimer's disease.Molecular neurodegeneration · 2022Review
- Rare missense mutations in ABCA7 might increase Alzheimer's disease risk by plasma membrane exclusion.Acta neuropathologica communications · 2022Article
- ABCA7 rs3764650 Polymorphism is Associated with Delayed Neurocognitive Recovery.Pharmacogenomics and personalized medicine · 2022Article
- Strategies to gain novel Alzheimer's disease diagnostics and therapeutics using modulators of ABCA transporters.Free neuropathology · 2021Article
- Lipids and Alzheimer's Disease.International journal of molecular sciences · 2020Review
- In vivo methods for acute modulation of gene expression in the central nervous system.Progress in neurobiology · 2018Review
- ABCA7 and Pathogenic Pathways of Alzheimer's Disease.Brain sciences · 2018Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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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Registered trials
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