ArticleBMC neuroscience2019
Amyloid-β plaque formation and reactive gliosis are required for induction of cognitive deficits in App knock-in mouse models of Alzheimer's disease.
Article in BMC neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 65 citations in OpenAlex.
- Restoration of Normal Occlusion Suppresses the Risk of Dementia.Neurochemical research · 2026Article
- Disrupted hippocampal replay is associated with reduced offline map stabilization in an Alzheimer's mouse model.Current biology : CB · 2026Article
- Can Panax ginseng help protect the body from the harmful effects of airborne particulate matter?Journal of ginseng research · 2025Review
- Beyond Transgenic Mice: Emerging Models and Translational Strategies in Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Impaired Cognitive Flexibility With Preserved Learning in an Amyloid Precursor Protein Knock-In Mouse Model of Amyloidopathy.Genes, brain, and behavior · 2025Article
- Commonly prescribed multi-medication therapies exert sex-specific effects on Alzheimer's disease pathology and metabolomic profiles in AppAlzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Longitudinal characterization reveals behavioral impairments in aged APP knock in mouse models.Scientific reports · 2025Article
- Structural Variations of Prions and Prion-like Proteins Associated with Neurodegeneration.Current issues in molecular biology · 2024Review
- Genetically modified non-human primate models for research on neurodegenerative diseases.Zoological research · 2024Review
- Modeling of age-related neurological disease: utility of zebrafish.Frontiers in aging neuroscience · 2024Review
- Inflammation as common link to progressive neurological diseases.Archives of toxicology · 2024Review
- Associations of amyloid-β oligomers and plaques with neuropathology in theBrain communications · 2024Article
- Soluble epoxide hydrolase inhibitor blockage microglial cell activation in subnucleus caudalis in a persistent model of arthritis.International immunopharmacology · 2023Article
- Caffeine protects against hippocampal alterations in type 2 diabetic rats via modulation of gliosis, inflammation and apoptosis.Cell and tissue research · 2023Article
- Impaired episodic-like memory in a mouse model of Alzheimer's disease is associated with hyperactivity in prefrontal-hippocampal regions.Disease models & mechanisms · 2023Article
- Alzheimer's Disease-Related Phospho-Tau181 Signals Are Localized to Demyelinated Axons of Parvalbumin-Positive GABAergic Interneurons in an App Knock-In Mouse Model of Amyloid-β Pathology.Journal of Alzheimer's disease : JAD · 2023Article
- Sex-split analysis of pathology and motor-behavioral outcomes in a mouse model of CLN8-Batten disease reveals an increased disease burden and trajectory in female Cln8Orphanet journal of rare diseases · 2022Article
- Novel App knock-in mouse model shows key features of amyloid pathology and reveals profound metabolic dysregulation of microglia.Molecular neurodegeneration · 2022Article
- Assessments of prolonged effects of desflurane and sevoflurane on motor learning deficits in aged AppMolecular brain · 2022Article
- Distinct brain pathologies associated with Alzheimer's disease biomarker-related phospho-tau 181 and phospho-tau 217 inBrain communications · 2022Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundKnock-in (KI) mouse models of Alzheimer's disease (AD) that endogenously overproduce Aβ without non-physiological overexpression of amyloid precursor protein (APP) provide important insights into the pathogenic mechanisms of AD. Previously, we reported that App
resultsIn the Morris water maze, a spatial task, 24-month-old App
conclusionsAβ plaque formation, followed by sustained neuroinflammation, is necessary for the induction of definitive cognitive deficits in App-KI mouse models of AD. Our data also indicate that introduction of the Swedish mutation alone in endogenous APP is not sufficient to produce either AD-related brain pathology or cognitive deficits in mice.
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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.