ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2025
Amyloid precursor protein and presenilin-1 knock-in immunodeficient mice exhibit intraneuronal Aβ pathology, microgliosis, and extensive neuronal loss.
Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 8 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed.
- Increased Amyloidogenic Neuronal Injury in HIV-1-infected APP-KI Alzheimer's disease mice.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Prostaglandins: Key players in immunomodulation of the nervous system.Neural regeneration research · 2026Article
- 5xFAD-NSG mice: a preclinical Alzheimer model for human cell therapy studies.bioRxiv : the preprint server for biology · 2026Article
- Molecular mechanisms of gut microbiota dysbiosis and metabolites in Alzheimer's disease pathogenesis: implications for precision therapeutics.Molecular brain · 2025Review
- Amyloid precursor protein and presenilin-1 knock-in immunodeficient mice exhibit intraneuronal Aβ pathology, microgliosis, and extensive neuronal loss.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Mitochondria Metabolism Regulates Glucose-Lipid Homeostasis in Neurodegenerative Diseases.Research (Washington, D.C.) · 2025Review
- Stem cell and CRISPR/Cas9 gene editing technology in Alzheimer's disease therapy: from basic research to clinical innovation.Frontiers in genome editing · 2025Review
- Stem-cell-derived extracellular vesicles in neurodegeneration and neuroaging: therapeutic potential and challenges.Extracellular vesicles and circulating nucleic acids · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
14 authors.
Funding
Abstract
introductionTransgenic mice overexpressing familial Alzheimer's disease (AD) mutations (FAD) show non-physiological traits, and their immunocompetent backgrounds limit their use in AD immunotherapy research. Preclinical models that reflect human immune responses in AD are needed.
methodsUsing CRISPR-Cas9, we developed single (NA) and double (NAPS) knock-in (KI) amyloid precursor protein (APP)
resultsBoth NA and NAPS mice developed pathology without overexpression artifacts. Mutation-induced upregulation of APP-CTF-β led to intraneuronal human amyloid beta (Aβ) (6E10) deposits and amyloid-associated microgliosis as early as 3 months, which increased with age. The addition of the PS 1 DISCUSSION: These models replicate intraneuronal amyloid pathology and, with human immune reconstitution potential, enable novel studies of human immune responses in AD. HIGHLIGHTS: A novel Alzheimer's disease (AD) knock-in (KI) mouse was developed and characterized on an immunodeficient NOG background. The model provides a platform for human immune studies and the evaluation of immunotherapies for AD. The KI mice demonstrate intraneuronal Aβ deposits and amyloid-associated microglial reactions. KI mice demonstrate extensive neuronal loss. Human immune reconstitution enables studies of infectious AD co-morbidities, such as the human immunodeficiency and herpes simplex viruses.
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What Socratic holds
Registered trials
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 Socratic graph.