Comprehensive evaluation of the 5xFAD mouse model for preclinical testing applications: A MODEL-AD study.
Open accessAbstract
The ability to investigate therapeutic interventions in animal models of neurodegenerative diseases depends on extensive characterization of the model(s) being used. There are numerous models that have been generated to study Alzheimer’s disease (AD) and the underlying pathogenesis of the disease. While transgenic models have been instrumental in understanding AD mechanisms and risk factors, they are limited in the degree of characteristics displayed in comparison with AD in humans, and the full spectrum of AD effects has yet to be recapitulated in a single mouse model. The Model Organism Development and Evaluation for Late-Onset Alzheimer’s Disease (MODEL-AD) consortium was assembled by the National Institute on Aging (NIA) to develop more robust animal models of AD with increased relevance to human disease, standardize the characterization of AD mouse models, improve preclinical testing in animals, and establish clinically relevant AD biomarkers, among other aims toward enhancing the translational value of AD models in clinical drug design and treatment development. Here we have conducted a detailed characterization of the 5XFAD mouse, including transcriptomics, electroencephalogram, in vivo imaging, biochemical characterization, and behavioral assessments. The data from this study is publicly available through the AD Knowledge Portal.
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In 5xFAD mice, amyloid plaques are first observed between two and four months of age in the cortical layer V and in the subiculum of the hippocampal formation.
“In 5xFAD mice, amyloid plaques are first observed between two and four months of age in the cortical layer V and in the subiculum of the hippocampal formation (Oblak et al., 2021).”
From Age-dependent microstructure alterations in 5xFAD mice by high-resolution diffusion tensor imaging (2022) · cites this paper as Oblak et al., 2021
The Results section, “Whole Brain Imaging and Quantification of Plaque Progression” (page not provided), reports plaques in 5XFAD mice by two months, with high densities in the hippocampal formation. It does not identify cortical layer V or the subiculum as the sites where plaques first appear; the separate mentions of those locations concern neuron loss, not initial plaque deposition. (LLM, conf=0.88)
Experimental — accuracy not yet measuredThere is robust Aβ deposition in the subiculum in 5xFAD animals.
“Given the robust Aβ deposition in the subiculum in 5xFAD animals, 16 we selected this region to analyze the morphology of diffuse (6E10 + , green) and dense-core (X34 + , blue) plaques, along with neuronal abundance using the neuronal nuclear protein (NeuN, red) in matched brain sections (Figure 2A).”
From <i>INPP5D</i> deficiency attenuates amyloid pathology in a mouse model of Alzheimer's disease (2023) · cites this paper as [16]
The Results section on whole-brain imaging reports that 5XFAD mice have high Aβ plaque densities in the hippocampal formation, which supports the general premise. It does not establish robust deposition specifically in the subiculum; the Results passage that names the subiculum concerns neuronal loss, not plaque density. Page numbers were not available in our copy. (LLM, conf=0.82)
Experimental — accuracy not yet measuredOur positive findings contrast sharply with negative findings of the MODEL-AD consortium and other recent studies that have also used T1/T2 MRI and DTI methods.
“Our positive findings contrast sharply with negative findings of the MODEL-AD consortium16 and other recent studies that have also used T1/T2 MRI and DTI methods7,44 (Supplementary Tables 2 and 3).”
From Magnetic resonance microscopy maps widespread effects of Alzheimer’s disease on brain structures and behavior in mice (2026) · cites this paper as [16]
The Materials and Methods section (Magnetic Resonance Imaging; page unavailable) confirms that this MODEL-AD study acquired T2-weighted MRI images. The cited passages do not report negative T1/T2 MRI or DTI findings: they describe T2 imaging for the PET/MRI work, while the Results report PET-detected changes. Thus the citation supports the study identification and T2 use, but not the attributed negative findings or use of T1 and DTI. (LLM, conf=0.82)
Experimental — accuracy not yet measuredThe possibility that rostral-to-caudal effects are downstream of regional differences in promoter activity can probably be ruled out because many teams have shown strong expression of the transgene and high levels of amyloid plaque deposition in thalamus and midbrain.
“This raises the possibility that rostral-to-caudal effects we have detected are downstream of regional differences in promoter activity. This can probably be ruled out because many teams have shown strong expression of the transgene and high levels of amyloid plaque deposition in thalamus and midbrain81—regions in which we have demonstrated highly significant reductions in volume (Ref20, their”
From Magnetic resonance microscopy maps widespread effects of Alzheimer’s disease on brain structures and behavior in mice (2026) · cites this paper as [16]
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Experimental — accuracy not yet measuredMice from both sexes were used unless otherwise specified; when both male and female mice were used, an analysis for sex differences was performed; unless otherwise noted, no sex differences were observed.
“Given the reported sex differences in some disease pathology phenotypes46,47,62, mice from both sexes were used unless otherwise specified. When both male and female mice were used, an analysis for sex differences was performed; unless otherwise noted, no sex differences were observed.”
From Lymphoid gene expression supports neuroprotective microglia function (2025) · cites this paper as [47]
5xFAD mice develop prominent gliosis, inflammation, neuronal loss, behavioral impairments, and sex-distinct systemic metabolic changes.
“5xFAD mice also develop prominent gliosis, inflammation, neuronal loss, behavioral impairments, and sex-distinct systemic metabolic changes39,38,40.”
From Amyloid-β induces lipid droplet-mediated microglial dysfunction via the enzyme DGAT2 in Alzheimer’s disease (2025) · cites this paper as [39]
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Tracing the Path between Mushrooms and Alzheimer’s Disease—A Literature Review
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- Authors
- Oblak, A. L., Lin, P. B., Kotredes, K. P., Pandey, R. S., Garceau, D., Williams, H. M., Uyar, A., O’Rourke, R., O’Rourke, S., Ingraham, C., Bednarczyk, D., Belanger, M., Cope, Z. A., Little, G. J., Williams, S.-P. G., Ash, C., Bleckert, A., Ragan, T., Logsdon, B. A., Mangravite, L. M., Sukoff Rizzo, S. J., Territo, P. R., Carter, G. W., Howell, G. R., Sasner, M., & Lamb, B. T.
- Affiliations
- Indiana University School of Medicine (US)
- Jackson Laboratory (US)
- University of Pittsburgh (US)
- The Jackson Laboratory for Genomic Medicine (US)
- Sage Bionetworks (US)
- Corresponding author
- Oblak, Adrian L.
- ORCID
- Venue
- Frontiers in Aging Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2021-07-23
- Volume
- 13
- Pages
- 713726-713726
- ISSN
- 1663-4365 (ISSN-L)
- PMC
- PMC8346252
- OpenAlex
- W3184377705
- Cited by
- 325
- References
- 92
- Citations by year
- 2026: 65 · 2025: 73 · 2024: 72 · 2023: 66 · 2022: 45 · 2021: 4
- FWCI
- 29.69
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Aging Neuroscience (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- The Mouseion at the JAXlibrary (Jackson Laboratory) (submittedVersion, cc-by)
- IUScholarWorks (Indiana University) (submittedVersion, cc-by)
- Purdue University Indianapolis (Indiana University) (submittedVersion, cc-by)
- Funders
- National Institute on Aging (U54AG054345, K01AG054753)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, transgenic mouse model, preclinical drug testing, model validation, transcriptomics, EEG, in vivo imaging, behavioral assessment, biomarkers, translational research
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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