ArticleBMC neuroscience2018
Cognitive and emotional alterations in App knock-in mouse models of Aβ amyloidosis.
Article in BMC neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
61 citing papers in PubMed, 80 citations in OpenAlex.
- Restoration of Normal Occlusion Suppresses the Risk of Dementia.Neurochemical research · 2026Article
- Article
- Immunotherapy with B28, an antibody to Aβ oligomers, potently decreases amyloid plaques, microgliosis, and memory decline in APP knock-in mice.Cell reports · 2026Article
- Age-Associated Behavioral Alterations in Laboratory-Housed Octodon degus.bioRxiv : the preprint server for biology · 2026Article
- Amyloid exacerbates tau and alpha-synuclein pathologies, behavioral impairments, and neuroinflammation in a mixed dementia model.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Altered trafficking of Kv1-Kvβ2 leads to neuronal hyperexcitability and memory deficits in amyloid-β pathology.Molecular neurodegeneration · 2026Article
- Operant House: A versatile open-source platform for automated operant conditioning testing of mice in home cages.PloS one · 2026Article
- Sleep-Wake Transitions Are Impaired in thebioRxiv : the preprint server for biology · 2025Article
- Amyloid Beta in Alzheimer's Disease: Mechanisms, Biomarker Potential, and Therapeutic Targets.CNS neuroscience & therapeutics · 2025Review
- Article
- Misclassification in memory modification ineLife · 2025Article
- Autophagic impairment in sleep-wake circuitry is linked to sleep loss at the early stages of Alzheimer's disease.Molecular neurodegeneration · 2025Article
- Impaired Cognitive Flexibility With Preserved Learning in an Amyloid Precursor Protein Knock-In Mouse Model of Amyloidopathy.Genes, brain, and behavior · 2025Article
- Modeling Alzheimer's Disease: A Review of Gene-Modified and Induced Animal Models, Complex Cell Culture Models, and Computational Modeling.Brain sciences · 2025Review
- A Novel APP Knock-In Mouse Model to Study the Protective Effects of the Icelandic Mutation In Vivo.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Evolution of Alzheimer's Disease Therapeutics: From Conventional Drugs to Medicinal Plants, Immunotherapy, Microbiotherapy and Nanotherapy.Pharmaceutics · 2025Review
- Non-invasive volumetric ultrasound localization microscopy detects vascular changes in mice with Alzheimer's disease.Theranostics · 2025Article
- Microglial cannabinoid receptor type II stimulation improves cognitive impairment and neuroinflammation in Alzheimer's disease mice by controlling astrocyte activation.Cell death & disease · 2024Article
- Primate-specific 82-kDa choline acetyltransferase attenuates progression of Alzheimer's disease-like pathology in the APPScientific reports · 2024Article
- Lost in translation: Inconvenient truths on the utility of mouse models in Alzheimer's disease research.eLife · 2024Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlzheimer's disease (AD), the most common cause of dementia, is characterized by the progressive deposition of amyloid-β (Aβ) peptides and neurofibrillary tangles. Mouse models of Aβ amyloidosis generated by knock-in (KI) of a humanized Aβ sequence provide distinct advantages over traditional transgenic models that rely on overexpression of amyloid precursor protein (APP). In App-KI mice, three familial AD-associated mutations were introduced into the endogenous mouse App locus to recapitulate Aβ pathology observed in AD: the Swedish (NL) mutation, which elevates total Aβ production; the Beyreuther/Iberian (F) mutation, which increases the Aβ42/Aβ40 ratio; and the Arctic (G) mutation, which promotes Aβ aggregation. App
resultsAssessments of emotional domains revealed that, in comparison with wild-type (WT) C57BL/6J mice, App
conclusionApp
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.