Insights on the Use of Transgenic Mice Models in Alzheimer’s Disease Research
Open accessAbstract
Alzheimer’s disease (AD), the leading cause of dementia, presents a significant global health challenge with no known cure to date. Central to our understanding of AD pathogenesis is the β-amyloid cascade hypothesis, which underlies drug research and discovery efforts. Despite extensive studies, no animal models of AD have completely validated this hypothesis. Effective AD models are essential for accurately replicating key pathological features of the disease, notably the formation of β-amyloid plaques and neurofibrillary tangles. These pathological markers are primarily driven by mutations in the amyloid precursor protein (APP) and presenilin 1 (PS1) genes in familial AD (FAD) and by tau protein mutations for the tangle pathology. Transgenic mice models have been instrumental in AD research, heavily relying on the overexpression of mutated APP genes to simulate disease conditions. However, these models do not entirely replicate the human condition of AD. This review aims to provide a comprehensive evaluation of the historical and ongoing research efforts in AD, particularly through the use of transgenic mice models. It is focused on the benefits gathered from these transgenic mice models in understanding β-amyloid toxicity and the broader biological underpinnings of AD. Additionally, the review critically assesses the application of these models in the preclinical testing of new therapeutic interventions, highlighting the gap between animal models and human clinical realities. This analysis underscores the need for refinement in AD research methodologies to bridge this gap and enhance the translational value of preclinical studies.
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Most preclinical studies have examined Aβ and tau in isolation using either Aβ amyloidosis models or tauopathy models.
“However, most preclinical studies have examined Aβ and tau in isolation, using either Aβ amyloidosis models that develop robust Aβ deposition without tau pathology, or tauopathy models that accumulate hyperphosphorylated tau in the absence of Aβ.”
From Unique transcriptomic alterations in 5XFAD;PS19 mouse model identify glial lipid dysregulation and coordinated microglial–oligodendrocyte responses (2026) · cites this paper as [10]
Section 2.3 says APP and APP/PS models lack neurofibrillary tangles, while its PS19 description reports tau tangles without β-amyloid deposits. These passages support the distinction between amyloid-focused and tau-focused models, but the review does not establish that most preclinical studies used them in isolation; it also describes models combining both pathologies. Page numbers are unavailable in our copy. (LLM, conf=0.84)
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Alzheimer’s disease and epilepsy: Research hotspots for comorbidity in the era of global aging
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Active immunization: A novel therapeutic strategy for treating Alzheimer's disease
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Retinal Degeneration in Alzheimer’s Disease 5xFAD Mice Fed DHA-Enriched Diets
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- Authors
- Pádua, M. S., Guil-Guerrero, J. L., Prates, J. A. M., & Lopes, P. A.
- Affiliations
- University of Lisbon (PT)
- Departamento de Tecnología de Alimentos, Universidad de Almería, 04120 Almería, Spain
- Corresponding author
- Lopes, Paula Alexandra
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2024-02-28
- Volume
- 25
- Issue
- 5
- Pages
- 2805
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC10931675
- OpenAlex
- W4392241116
- Semantic Scholar
- bbf22b1276a842e9d2e09911d7e14c840eff28d1
- Cited by
- 46
- References
- 154
- Citations by year
- 2026: 15 · 2025: 21 · 2024: 10
- FWCI
- 2.61
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Fundação para a Ciência e a Tecnologia (UIDB/00276/2020, LA/P/0059/2020, FCT.2022.08133.PTDC)
- FCT Stimulus of Scientific Employment Program (UIDB/00276/2020, LA/P/0059/2020, FCT.2022.08133.PTDC)
- 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, amyloid precursor protein, presenilin 1, familial Alzheimer's disease, tau protein, amyloid plaques, neurofibrillary tangles, amyloid-beta toxicity, preclinical drug testing, translational research, animal model limitations
- MeSH terms
- Alzheimer Disease, Animals, Disease Models, Animal, Humans, Mice, Transgenic, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, tau Proteins, Mice, Presenilin-1, Plaque, Amyloid
About these checks
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.
Statistics and arithmetic are recomputed, not judged.
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