Mouse models of Alzheimer’s disease
Abstract
Alzheimer's disease (AD) is a neurodegenerative disorder that nowadays affects more than 40 million people worldwide and it is predicted to exponentially increase in the coming decades. Because no curative treatment exists, research on the pathophysiology of the disease, as well as the testing of new drugs, are mandatory. For these purposes, animal models constitute a valuable, although perfectible tool. This review takes a tour through several aspects of mouse models of AD, such as the generation of transgenic models, the relevance of the promoter driving the expression of the transgenes, and the concrete transgenes used to simulate AD pathophysiology. Then, transgenic mouse lines harboring mutated human genes at several loci such as APP, PSEN1, APOEɛ4, and ob (leptin) are reviewed. Therefore, not only the accumulation of the Aβ peptide is emulated but also cholesterol and insulin metabolism. Further novel information about the disease will allow for the development of more accurate animal models, which in turn will undoubtedly be helpful for bringing preclinical research closer to clinical trials in humans.
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The most widely used transgenic models express mutant forms of APP, with or without PSEN1/2, associated with autosomal-dominant early-onset AD, or MAPT mutations, which cause familial frontotemporal dementia.
“The most widely used transgenic models express mutant forms of the amyloid precursor protein (APP) gene, with or without presenilin-1/2 (PSEN1/2), which are associated with autosomal-dominant, early-onset AD, or, alternatively, MAPT mutations, which cause familial frontotemporal dementia (FTD).”
From Meta-Analysis of the Alzheimer’s Disease Human Brain Transcriptome and Functional Dissection in Mouse Models (2020) · cites this paper as Esquerda-Canals et al., 2017
These models recapitulate features of AD neuropathology, including plaques or tangles, along with variable neuronal dysfunction or loss and progressive behavioral impairment.
“These models recapitulate features of AD neuropathology, including plaques or tangles, along with variable degree of neuronal dysfunction or loss and progressive behavioral impairment (Ballatore et al., 2007; Esquerda-Canals et al., 2017).”
From Meta-Analysis of the Alzheimer’s Disease Human Brain Transcriptome and Functional Dissection in Mouse Models (2020) · cites this paper as Esquerda-Canals et al., 2017
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- Authors
- Esquerda-Canals, G., Montoliu-Gaya, L., Güell-Bosch, J., & Villegas, S.
- Affiliations
- Universitat Autònoma de Barcelona (ES)
- Protein Folding and Stability Group, Departament de Bioquímica i Biologia Molecular, Facultat de Biociències, Universitat Autònoma de Barcelona, Cerdanyola del Vallès, Spain
- Corresponding author
- Villegas, Sandra
- ORCID
- Villegas, Sandra
- Venue
- Journal of Alzheimer’s Disease
- Publisher
- SAGE Publications
- Published
- 2017-03-10
- Volume
- 57
- Issue
- 4
- Pages
- 1171-1183
- ISSN
- 1387-2877 (ISSN-L)
- 1875-8908
- OpenAlex
- W2607050832
- Cited by
- 288
- References
- 20
- Citations by year
- 2026: 14 · 2025: 27 · 2024: 38 · 2023: 32 · 2022: 44 · 2021: 64 · 2020: 35 · 2019: 16 · 2018: 12 · 2017: 5 · 2016: 1
- FWCI
- 2.28
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Alzheimer s Disease (publishedVersion)
- PubMed (publishedVersion)
- 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, mouse model
- MeSH terms
- Alzheimer Disease, Animals, Disease Models, Animal, Humans, Mice, Transgenic
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