ArticlePloS one2013
A shortened Barnes maze protocol reveals memory deficits at 4-months of age in the triple-transgenic mouse model of Alzheimer's disease.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.
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Who cites it
97 citing papers in PubMed.
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- Select microbial metabolites promote tau aggregation in a murine tauopathy model.Nature communications · 2026Article
- ALKBH3 m1A Demethylase Deficiency Reduces Alzheimer's Amyloid-β Pathology.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Blocking microglial reactivity via purinergic receptors prevents subacute cognitive deficits after TIA.EMBO molecular medicine · 2026Article
- Suppression of haptoglobin and loss of striatal neurons in mice chronically exposed to chlorpyrifos-contaminated drinking water.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Neuronal alkaline phosphatase promotes the spread of Tau-induced pathology, and its blockade prevents neurodegeneration and memory loss.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Impact of chronic alcohol and stress on midlife cognition and locus coeruleus integrity in mice.Alcohol, clinical & experimental research · 2026Article
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- Impact of chronic alcohol and stress on mid-life cognition and locus coeruleus integrity.bioRxiv : the preprint server for biology · 2025Article
- Genotype and microbiome shape immunity in a sex-specific manner in mouse models of Alzheimer's disease.Brain, behavior, and immunity · 2025Article
- MT1-MMP inhibition rejuvenates ageing brain and rescues cognitive deficits in obesity.Cell discovery · 2025Article
- Neurovascular coupling and functional connectivity changes through the Alzheimer's disease spectrum: Effects of simvastatin treatment.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Amyloid-β plaque-associated microglia drive TSPO upregulation in Alzheimer's disease.Acta neuropathologica · 2025Article
- The MR1/MAIT cell axis impacts the gut-brain axis through both cognition and microbial community structure in 5XFAD mice.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Ivermectin's neuroprotective effects decrease with prolonged use after cerebral ischemia/reperfusion.Metabolic brain disease · 2025Article
- Beyond Transgenic Mice: Emerging Models and Translational Strategies in Alzheimer's Disease.International journal of molecular sciences · 2025Review
37 more citing papers are in PubMed but not listed here.
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7 authors.
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Abstract
Alzheimer's disease is a progressive neurodegenerative disease that manifests as memory loss, cognitive dysfunction, and dementia. Animal models of Alzheimer's disease have been instrumental in understanding the underlying pathological mechanism and in evaluation of potential therapies. The triple transgenic (3 × Tg) mouse model of AD is unique because it recapitulates both pathologic hallmarks of Alzheimer's disease--amyloid plaques and neurofibrillary tangles. The earliest cognitive deficits in this model have been shown at 6-m of age by most groups, necessitating aging of the mice to this age before initiating evaluation of the cognitive effects of therapies. To assess cognitive deficits in the 3 × Tg mice, originally we employed a typical Barnes maze protocol of 15 training trials, but found no significant deficits in aged mice. Therefore, we shortened the protocol to include only 5 training trials to increase difficulty. We found cognitive deficits using this protocol using mainly measures from the probe day, rather than the training trials. This also decreased the effort involved with data analysis. We compared 3 × Tg and wild-type mice at 4-m- and 15-m of age using both the original, long training, and the short training paradigms. We found that differences in learning between 3 × Tg and wild-type mice disappeared after the 4(th) training trial. Measures of learning and memory on the probe day showed significant differences between 3 × Tg and wild-type mice following the short, 5-training trial protocol but not the long, 15-training trial protocol. Importantly, we detected cognitive dysfunction already at 4-m of age in 3 × Tg mice using the short Barnes-maze protocol. The ability to test learning and memory in 4-m old 3 × Tg mice using a shortened Barnes maze protocol offers considerable time and cost savings and provides support for the utilization of this model at pre-pathology stages for therapeutic studies.
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