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Insights From TgF344-AD, a Double Transgenic Rat Model in Alzheimer’s Disease Research
Andrew Nataraj, Karel Blahna, Karel Ježek. Physiological Research, 2025-03-10
Topic: Brain proteins, microglia and lab models
Plain-language summary
Alzheimer's disease (AD), a leading cause of dementia worldwide, is a multifactorial neurodegenerative disorder characterized by amyloid-beta plaques, tauopathy, neuronal loss, neuro-inflammation, brain atrophy, and cognitive deficits. AD manifests as familial early-onset (FAD) with specific gene mutations or sporadic late-onset (LOAD) caused by various genetic and environmental factors. Numerous transgenic rodent models have been developed to understand AD pathology development and progression. The TgF344-AD rat model is a double transgenic model that carries two human gene mutations: APP with the Swedish mutation and PSEN-1 with delta exon 9 mutations. This model exhibits a complete repertoire of AD pathology in an age-dependent manner. This review summarizes multidisciplinary research insights gained from studying TgF344-AD rats in the context of AD pathology. We explore neuropathological findings; electrophysiological assessments revealing disrupted synaptic transmission, reduced spatial coding, network-level dysfunctions, and altered sleep architecture; behavioral studies highlighting impaired spatial memory; alterations in excitatory-inhibitory systems; and molecular and physiological changes in TgF344-AD rats emphasizing their age-related effects. Additionally, the impact of various interventions studied in the model is compiled, underscoring their role in bridging gaps in understanding AD pathogenesis. The TgF344-AD rat model offers significant potential in identifying biomarkers for early detection and therapeutic interventions, providing a robust platform for advancing translational AD research. Key words Alzheimer's disease, Transgenic AD models, TgF344-AD rats, Spatial coding.
What this study adds
Evidence grade: Low
This review describes a rat model that carries two human gene mutations and develops Alzheimer's-like pathology with age, which researchers can use to study the disease. It does not report a treatment or cure, but says the model may help identify biomarkers for early detection and test potential therapies.
Taken from this record’s own fields, not from reading the paper. The grade is assigned from the abstract’s wording; what that means.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Nataraj, A., Blahna, K., & Ježek, K. (2025). Insights From TgF344-AD, a Double Transgenic Rat Model in Alzheimer’s Disease Research. Physiological Research. https://doi.org/10.33549/physiolres.935464
Vancouver
Nataraj A, Blahna K, Ježek K. Insights From TgF344-AD, a Double Transgenic Rat Model in Alzheimer’s Disease Research. Physiological Research. 2025. doi:10.33549/physiolres.935464. PMID: 40116546.
BibTeX
@article{nataraj2025-40116546,
author = {Nataraj, Andrew and Blahna, Karel and Ježek, Karel},
title = {{Insights From TgF344-AD, a Double Transgenic Rat Model in Alzheimer’s Disease Research}},
journal = {Physiological Research},
year = {2025},
doi = {10.33549/physiolres.935464},
pmid = {40116546},
url = {https://doi.org/10.33549/physiolres.935464}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
Key findings
- The TgF344-AD rat model offers significant potential in identifying biomarkers for early detection and therapeutic interventions, providing a robust platform for advancing translational AD research.
Why it matters
This review describes a rat model that carries two human gene mutations and develops Alzheimer's-like pathology with age, which researchers can use to study the disease. It does not report a treatment or cure, but says the model may help identify biomarkers for early detection and test potential therapies.
Study details
- Evidence strengthLow
How this study scored 37/100
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.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Physiological Research) |
| Journal's citation record | 1 / 4 | Physiological Research: journal h-index 96 (OpenAlex, 2026-10-29) |
| 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 | 4 / 5 | 2025 — within 3 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 | 2 / 7 | Cited 10 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 3.3 citations a year over 3 year(s) since 2025 |
| Impact for its field and year | 3 / 6 | Cited 5.5× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 1 / 4 | Cited 10 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 1 / 4 | Last-listed author Karel Ježek: h-index 14 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Charles University: institution h-index 721 (OpenAlex) |
| Multicenter collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 40116546) |
| Free to read | 2 / 2 | Free to read |
| Total | 37 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.33549/physiolres.935464
- PubMed: 40116546
- Original source →
- Free full text: Physiological Research →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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