Transgenic Mouse Models of Alzheimer’s Disease: An Integrative Analysis
Alzheimer’s disease (AD) constitutes the most prominent form of dementia among elderly individuals worldwide. Disease modeling using murine transgenic mice was first initiated thanks to the discovery of heritable mutations in amyloid precursor protein (APP) and presenilins (PS) genes. However, due t...
| Main Authors: | , , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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MDPI AG
2022-05-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/23/10/5404 |
| _version_ | 1797499278958002176 |
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| author | Raquel Sanchez-Varo Marina Mejias-Ortega Juan Jose Fernandez-Valenzuela Cristina Nuñez-Diaz Laura Caceres-Palomo Laura Vegas-Gomez Elisabeth Sanchez-Mejias Laura Trujillo-Estrada Juan Antonio Garcia-Leon Ines Moreno-Gonzalez Marisa Vizuete Javier Vitorica David Baglietto-Vargas Antonia Gutierrez |
| author_facet | Raquel Sanchez-Varo Marina Mejias-Ortega Juan Jose Fernandez-Valenzuela Cristina Nuñez-Diaz Laura Caceres-Palomo Laura Vegas-Gomez Elisabeth Sanchez-Mejias Laura Trujillo-Estrada Juan Antonio Garcia-Leon Ines Moreno-Gonzalez Marisa Vizuete Javier Vitorica David Baglietto-Vargas Antonia Gutierrez |
| author_sort | Raquel Sanchez-Varo |
| collection | DOAJ |
| description | Alzheimer’s disease (AD) constitutes the most prominent form of dementia among elderly individuals worldwide. Disease modeling using murine transgenic mice was first initiated thanks to the discovery of heritable mutations in amyloid precursor protein (APP) and presenilins (PS) genes. However, due to the repeated failure of translational applications from animal models to human patients, along with the recent advances in genetic susceptibility and our current understanding on disease biology, these models have evolved over time in an attempt to better reproduce the complexity of this devastating disease and improve their applicability. In this review, we provide a comprehensive overview about the major pathological elements of human AD (plaques, tauopathy, synaptic damage, neuronal death, neuroinflammation and glial dysfunction), discussing the knowledge that available mouse models have provided about the mechanisms underlying human disease. Moreover, we highlight the pros and cons of current models, and the revolution offered by the concomitant use of transgenic mice and omics technologies that may lead to a more rapid improvement of the present modeling battery. |
| first_indexed | 2024-03-10T03:45:10Z |
| format | Article |
| id | doaj.art-2fc137a7578741d99a3f0159b3e90e28 |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-10T03:45:10Z |
| publishDate | 2022-05-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-2fc137a7578741d99a3f0159b3e90e282023-11-23T11:22:05ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672022-05-012310540410.3390/ijms23105404Transgenic Mouse Models of Alzheimer’s Disease: An Integrative AnalysisRaquel Sanchez-Varo0Marina Mejias-Ortega1Juan Jose Fernandez-Valenzuela2Cristina Nuñez-Diaz3Laura Caceres-Palomo4Laura Vegas-Gomez5Elisabeth Sanchez-Mejias6Laura Trujillo-Estrada7Juan Antonio Garcia-Leon8Ines Moreno-Gonzalez9Marisa Vizuete10Javier Vitorica11David Baglietto-Vargas12Antonia Gutierrez13Departamento Biologia Celular, Genetica y Fisiologia, Instituto de Investigacion Biomedica de Malaga-IBIMA, Facultad de Ciencias, Universidad de Malaga, 29071 Malaga, SpainDepartamento Biologia Celular, Genetica y Fisiologia, Instituto de Investigacion Biomedica de Malaga-IBIMA, Facultad de Ciencias, Universidad de Malaga, 29071 Malaga, SpainDepartamento Biologia Celular, Genetica y Fisiologia, Instituto de Investigacion Biomedica de Malaga-IBIMA, Facultad de Ciencias, Universidad de Malaga, 29071 Malaga, SpainDepartamento Biologia Celular, Genetica y Fisiologia, Instituto de Investigacion Biomedica de Malaga-IBIMA, Facultad de Ciencias, Universidad de Malaga, 29071 Malaga, SpainDepartamento Biologia Celular, Genetica y Fisiologia, Instituto de Investigacion Biomedica de Malaga-IBIMA, Facultad de Ciencias, Universidad de Malaga, 29071 Malaga, SpainDepartamento Biologia Celular, Genetica y Fisiologia, Instituto de Investigacion Biomedica de Malaga-IBIMA, Facultad de Ciencias, Universidad de Malaga, 29071 Malaga, SpainDepartamento Biologia Celular, Genetica y Fisiologia, Instituto de Investigacion Biomedica de Malaga-IBIMA, Facultad de Ciencias, Universidad de Malaga, 29071 Malaga, SpainDepartamento Biologia Celular, Genetica y Fisiologia, Instituto de Investigacion Biomedica de Malaga-IBIMA, Facultad de Ciencias, Universidad de Malaga, 29071 Malaga, SpainDepartamento Biologia Celular, Genetica y Fisiologia, Instituto de Investigacion Biomedica de Malaga-IBIMA, Facultad de Ciencias, Universidad de Malaga, 29071 Malaga, SpainDepartamento Biologia Celular, Genetica y Fisiologia, Instituto de Investigacion Biomedica de Malaga-IBIMA, Facultad de Ciencias, Universidad de Malaga, 29071 Malaga, SpainCentro de Investigacion Biomedica en Red Sobre Enfermedades Neurodegenerativas (CIBERNED), 28031 Madrid, SpainCentro de Investigacion Biomedica en Red Sobre Enfermedades Neurodegenerativas (CIBERNED), 28031 Madrid, SpainDepartamento Biologia Celular, Genetica y Fisiologia, Instituto de Investigacion Biomedica de Malaga-IBIMA, Facultad de Ciencias, Universidad de Malaga, 29071 Malaga, SpainDepartamento Biologia Celular, Genetica y Fisiologia, Instituto de Investigacion Biomedica de Malaga-IBIMA, Facultad de Ciencias, Universidad de Malaga, 29071 Malaga, SpainAlzheimer’s disease (AD) constitutes the most prominent form of dementia among elderly individuals worldwide. Disease modeling using murine transgenic mice was first initiated thanks to the discovery of heritable mutations in amyloid precursor protein (APP) and presenilins (PS) genes. However, due to the repeated failure of translational applications from animal models to human patients, along with the recent advances in genetic susceptibility and our current understanding on disease biology, these models have evolved over time in an attempt to better reproduce the complexity of this devastating disease and improve their applicability. In this review, we provide a comprehensive overview about the major pathological elements of human AD (plaques, tauopathy, synaptic damage, neuronal death, neuroinflammation and glial dysfunction), discussing the knowledge that available mouse models have provided about the mechanisms underlying human disease. Moreover, we highlight the pros and cons of current models, and the revolution offered by the concomitant use of transgenic mice and omics technologies that may lead to a more rapid improvement of the present modeling battery.https://www.mdpi.com/1422-0067/23/10/5404Alzheimer’s diseasetransgenic miceamyloidtaumicrogliaastrocytes |
| spellingShingle | Raquel Sanchez-Varo Marina Mejias-Ortega Juan Jose Fernandez-Valenzuela Cristina Nuñez-Diaz Laura Caceres-Palomo Laura Vegas-Gomez Elisabeth Sanchez-Mejias Laura Trujillo-Estrada Juan Antonio Garcia-Leon Ines Moreno-Gonzalez Marisa Vizuete Javier Vitorica David Baglietto-Vargas Antonia Gutierrez Transgenic Mouse Models of Alzheimer’s Disease: An Integrative Analysis International Journal of Molecular Sciences Alzheimer’s disease transgenic mice amyloid tau microglia astrocytes |
| title | Transgenic Mouse Models of Alzheimer’s Disease: An Integrative Analysis |
| title_full | Transgenic Mouse Models of Alzheimer’s Disease: An Integrative Analysis |
| title_fullStr | Transgenic Mouse Models of Alzheimer’s Disease: An Integrative Analysis |
| title_full_unstemmed | Transgenic Mouse Models of Alzheimer’s Disease: An Integrative Analysis |
| title_short | Transgenic Mouse Models of Alzheimer’s Disease: An Integrative Analysis |
| title_sort | transgenic mouse models of alzheimer s disease an integrative analysis |
| topic | Alzheimer’s disease transgenic mice amyloid tau microglia astrocytes |
| url | https://www.mdpi.com/1422-0067/23/10/5404 |
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