ReviewCellular and molecular neurobiology2026
The 3xTg-AD Mouse Model: A Comprehensive Tool for Understanding Alzheimer's Disease.
Review in Cellular and molecular neurobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Who cites it
6 citing papers in PubMed.
- Article
- Andrographolide: Mechanisms and Therapeutic Potential in Alzheimer's and Parkinson's Disease.Molecules (Basel, Switzerland) · 2026Review
- Peripheral and Central miRNA Signatures in Alzheimer's Disease: Tissue-Specific Variability, Sex-Associated Differences, and Implications for Blood-Based Biomarkers.International journal of molecular sciences · 2026Review
- Kilovoltage Energy Significantly Enhances the Therapeutic Efficacy of Low-Dose Radiation in a 3xTg-AD Mouse Model of Alzheimer's Disease.International journal of molecular sciences · 2026Article
- A novel PGK1 activator improves Alzheimer's disease by regulating glycolysis.Alzheimer's research & therapy · 2026Article
- Dynamic changes of gut microbiota during progression of three Alzheimer's disease mice models.Frontiers in neuroscience · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is an evolving neurodegenerative disorder characterized by the presence of Amyloid-β (Aβ) plaques, neurofibrillary tangles (NFTs), synaptic dysfunction, neuroinflammation, and decline in memory. Animal models are crucial resources for examining AD processes and evaluating potential treatments. Triple-transgenic mice (3xTg-AD) are genetically altered to overexpress tau, PSEN1, and APP, three genes linked to AD in humans. Both tau and amyloid pathologies are independently replicated in each model in an age-related, temporal sequence that mimics the pathophysiology of AD in humans. In addition to synaptic damage, neuroinflammation, and cognitive deficits, these mice develop intracellular Aβ accumulations at 3 to 4 months, extracellular plaques at 6 to 9 months, and NFTs at 12 months. Additionally, the model exhibits sex-dependent differences and non-cognitive symptoms like anxiety and depressive-like behavior. Recent study indicates its potential in evaluating immunotherapy, irradiation, nutraceuticals such resveratrol and lifestyle therapies for the decrease of Aβ, and tau deposition and improved cognition. Additionally, neuroimaging, and multi-omics analysis in 3xTg-AD mice provide useful biomarkers for disease monitoring. The limitations of 3xTg-AD mice include their shorter lifetime, sex-specific variations in disease and behavior and the inaccurate timing of symptom onset relative to humans. The pathological and behavioral characteristics of the 3xTg-AD mouse are well understood, but this review highlights its developing translational potential. Further studies highlight that how preclinical findings can be connected to human AD by utilizing multi-omics profiling, CRISPR-mediated genetic refinement, and integration with human iPSC-derived systems. Hence, the 3xTg-AD mouse is an effective and versatile model for studying AD processes as well as preclinical therapeutic approaches.
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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.