ArticleNature communications2018
Generation of App knock-in mice reveals deletion mutations protective against Alzheimer's disease-like pathology.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 50 citations in OpenAlex.
- CRISPR Applications in Alzheimer's Disease: From High-Throughput Genetic Screening to Precision Editing and CNS Delivery.International journal of molecular sciences · 2026Review
- Trends and challenges of AAV-delivered gene editing therapeutics for CNS disorders: Implications for neurodegenerative disease.Molecular therapy. Nucleic acids · 2025Review
- CRISPR/Cas9-Based therapeutics as a promising strategy for management of Alzheimer's disease: progress and prospects.Frontiers in cellular neuroscience · 2025Review
- Application of CRISPR/Cas9 System in the Treatment of Alzheimer's Disease and Neurodegenerative Diseases.Molecular neurobiology · 2024Review
- Role and application of CRISPR-Cas9 in the management of Alzheimer's disease.Annals of medicine and surgery (2012) · 2024Review
- A society-wide conversation is needed about germline genome editing using CRISPR.Nature medicine · 2024Article
- Neuroimaging techniques, gene therapy, and gut microbiota: frontier advances and integrated applications in Alzheimer's Disease research.Frontiers in aging neuroscience · 2024Review
- CRISPR/Cas9 Gene Editing: A Novel Approach Towards Alzheimer's Disease Treatment.CNS & neurological disorders drug targets · 2024Review
- Using Stems to Bear Fruit: Deciphering the Role of Alzheimer's Disease Risk Loci in Human-Induced Pluripotent Stem Cell-Derived Microglia.Biomedicines · 2023Review
- Vector enabled CRISPR gene editing - A revolutionary strategy for targeting the diversity of brain pathologies.Coordination chemistry reviews · 2023Article
- Advances in CRISPR therapeutics.Nature reviews. Nephrology · 2023Review
- CRISPR/Cas9 gene editing: New hope for Alzheimer's disease therapeutics.Journal of advanced research · 2022Review
- Applications of CRISPR-Cas9 in Alzheimer's Disease and Related Disorders.International journal of molecular sciences · 2022Review
- Exploring the Involvement of the Amyloid Precursor Protein A673T Mutation against Amyloid Pathology and Alzheimer's Disease in Relation to Therapeutic Editing Tools.Pharmaceutics · 2022Review
- Brain-wide Cas9-mediated cleavage of a gene causing familial Alzheimer's disease alleviates amyloid-related pathologies in mice.Nature biomedical engineering · 2022Article
- Gene Therapy Approach with an Emphasis on Growth Factors: Theoretical and Clinical Outcomes in Neurodegenerative Diseases.Molecular neurobiology · 2022Review
- Recent Advances in the Modeling of Alzheimer's Disease.Frontiers in neuroscience · 2022Review
- Application of CRISPR/Cas9 in Alzheimer's Disease.Frontiers in neuroscience · 2021Review
- Gene Therapy for Neurodegenerative Disease: Clinical Potential and Directions.Frontiers in molecular neuroscience · 2021Review
- A comprehensive guide to studying inflammasome activation and cell death.Nature protocols · 2020Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although, a number of pathogenic mutations have been found for Alzheimer's disease (AD), only one protective mutation has been identified so far in humans. Here we identify possible protective deletion mutations in the 3'-UTR of the amyloid precursor protein (App) gene in mice. We use an App knock-in mouse model carrying a humanized Aβ sequence and three AD mutations in the endogenous App gene. Genome editing of the model zygotes using multiple combinations of CRISPR/Cas9 tools produces genetically mosaic animals with various App 3'-UTR deletions. Depending on the editing efficiency, the 3'-UTR disruption mitigates the Aβ pathology development through transcriptional and translational regulation of APP expression. Notably, an App knock-in mouse with a 34-bp deletion in a 52-bp regulatory element adjacent to the stop codon shows a substantial reduction in Aβ pathology. Further functional characterization of the identified element should provide deeper understanding of the pathogenic mechanisms of AD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.