Home › Research › Disease mechanisms
Transgenic Mouse Models of Alzheimer's Disease: An Integrative Analysis
Sanchez-Varo R, Mejias-Ortega M, Fernandez-Valenzuela JJ, Nuñez-Diaz C, Caceres-Palomo L, Vegas-Gomez L, Sanchez-Mejias E, Trujillo-Estrada L et al.. International journal of molecular sciences, 2022-05-12
Topic: Amyloid, tau and blood-test diagnosis
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.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Sanchez-Varo, R., Mejias-Ortega, M., Fernandez-Valenzuela, J. J., Nuñez-Diaz, C., Caceres-Palomo, L., Vegas-Gomez, L., et al. (2022). Transgenic Mouse Models of Alzheimer's Disease: An Integrative Analysis. International journal of molecular sciences. https://doi.org/10.3390/ijms23105404
Vancouver
Sanchez-Varo R, Mejias-Ortega M, Fernandez-Valenzuela JJ, Nuñez-Diaz C, Caceres-Palomo L, Vegas-Gomez L, et al. Transgenic Mouse Models of Alzheimer's Disease: An Integrative Analysis. International journal of molecular sciences. 2022. doi:10.3390/ijms23105404. PMID: 35628216.
BibTeX
@article{sanchezvaro2022-35628216,
author = {Sanchez-Varo, R. and Mejias-Ortega, M. and Fernandez-Valenzuela, J. J. and Nuñez-Diaz, C. and Caceres-Palomo, L. and Vegas-Gomez, L. and Sanchez-Mejias, E. and Trujillo-Estrada, L. and others},
title = {{Transgenic Mouse Models of Alzheimer's Disease: An Integrative Analysis}},
journal = {International journal of molecular sciences},
year = {2022},
doi = {10.3390/ijms23105404},
pmid = {35628216},
url = {https://doi.org/10.3390/ijms23105404}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.
Key findings
- 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.
Study details
- Evidence strengthLow
How this study scored 43/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomized / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multicenter collaboration, so those were left out: it earned 25 of the 58 points we could judge it on, which is 43 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (International journal of molecular sciences) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 3 / 5 | 2022 — within 6 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Laboratory or animal study (title names “transgenic”) — scores zero |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multicenter collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 35628216) |
| Free to read | 2 / 2 | Free to read |
| Points | 25 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 25 of the 58 points we could judge it on is 43 out of 100. |
| Total | 43 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
Free copy unknown: no free-copy check has an answer for this record yet. That does not mean it is paywalled.
Related
Studies in the library that share something with this one. The line above each title says what.
Related studies in Disease mechanisms
Also in Disease mechanisms
128 studies in the library are filed under Disease mechanisms with no topic tag they share with another; these are this study's neighbours in a fixed tour of them. The Disease mechanisms hub.