Transgenic mouse models of Alzheimer’s disease.

Elder, Gregory A.; Gama Sosa, Miguel A.; De Gasperi, Rita

doi:10.1002/msj.20159

Cited by 336Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Transgenic mouse models of Alzheimer’s disease.

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Elder, Gregory A., Gama Sosa, Miguel A., De Gasperi, Rita·2010·Mount Sinai Journal of Medicine A Journal of Translational and Personalized Medicine

DOI 10.1002/msj.20159PMC PMC2925685

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Abstract

Alzheimer's disease is the most common cause of senile dementia in the United States and Europe. At present, there is no effective treatment. Given the disease's prevalence and poor prognosis, the development of animal models has been a high research priority. Transgenic modeling has been pursued on the basis of the amyloid hypothesis and has taken advantage of mutations in the amyloid precursor protein and the presenilins that cause familial forms of Alzheimer's disease. Modeling has been most aggressively pursued in mice, for which the techniques of genetic modification are well developed. Transgenic mouse models now exist that mimic a range of Alzheimer's disease-related pathologies. Although none of the models fully replicates the human disease, the models have contributed significant insights into the pathophysiology of beta-amyloid toxicity, particularly with respect to the effects of different beta-amyloid species and the possible pathogenic role of beta-amyloid oligomers. They have also been widely used in the preclinical testing of potential therapeutic modalities and have played a pivotal role in the development of immunotherapies for Alzheimer's disease that are currently in clinical trials. These models will, without a doubt, continue to play central roles in preclinical testing and be used as tools for developing insights into the biological basis of Alzheimer's disease.

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The degree of characteristics displayed by transgenic models in comparison with AD in humans is still limited.
“the degree of characteristics displayed in comparison with AD in humans is still limited (Elder et al., 2010).”
From Age-dependent microstructure alterations in 5xFAD mice by high-resolution diffusion tensor imaging (2022) · cites this paper as Elder et al., 2010
Transgenic models have been widely used to study AD risk factors and mechanisms.
“transgenic models have been widely used to study AD risk factors and mechanisms”
From Age-dependent microstructure alterations in 5xFAD mice by high-resolution diffusion tensor imaging (2022) · cites this paper as Elder et al., 2010
The most commonly used murine models of Alzheimer's disease do not exhibit disease-related neuronal loss.
“The most commonly used murine models of AD do not exhibit disease-related neuronal loss15.”
From Neuronally-directed effects of RXR activation in a mouse model of Alzheimer’s disease (2017) · cites this paper as [15]

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“factors and mechanisms, but the degree of characteristics displayed in comparison with AD in humans is still limited (Elder et al., 2010).”
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Authors: Elder, G. A., Gama Sosa, M. A., & De Gasperi, R.
Affiliations: James J. Peters VA Medical Center (US)
Corresponding author: Elder, Gregory A.
ORCID: Elder, Gregory A.
Venue: Mount Sinai Journal of Medicine A Journal of Translational and Personalized Medicine
Publisher: Wiley
Published: 2010-01
Volume: 77
Issue: 1
Pages: 69-81
ISSN: 0027-2507 (ISSN-L)
1931-7581
DOI: 10.1002/msj.20159
PMC: PMC2925685
OpenAlex: W2098977708
Cited by: 336
References: 104
Citations by year: 2026: 6 · 2025: 12 · 2024: 21 · 2023: 27 · 2022: 27 · 2021: 27 · 2020: 23 · 2019: 36 · 2018: 22 · 2017: 36 · 2016: 17 · 2015: 20 · 2014: 18 · 2013: 10 · 2012: 15
FWCI: 1.38
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor, 24 d)
Locations: Mount Sinai Journal of Medicine A Journal of Translational and Personalized Medicine (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: U.S. Department of Veterans Affairs (I01 BX000342)
National Institute on Aging (AG029361, AG-02219, AG 05138, P50AG005138, AG20139, R21AG029361, P01AG002219, R01AG020139)
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 hypothesis, amyloid precursor protein, presenilin, familial Alzheimer's disease, amyloid-beta toxicity, amyloid-beta oligomers, immunotherapy, preclinical drug testing, senile dementia
MeSH terms: Alzheimer Disease, Animals, Disease Models, Animal, Humans, Mice, Transgenic, Mutation, Amyloid beta-Protein Precursor, Mice, Presenilins

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