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Enhanced oxidative stress is an early event during development of Alzheimer-like pathologies in presenilin conditional knock-out mice
Gu F, Zhu M, Shi J, Hu Y, Zhao Z.. Neuroscience letters, 2008-05-18
Topic: Brain proteins, microglia and lab models
Conditional double knock-out of presenilin-1 (PS1) and presenilin-2 (PS2) (PS cDKO) in forebrain of mice led to progressive memory dysfunction and forebrain degeneration. These changes in the brain recapitulated most of the neurodegenerative phenotypes of Alzheimer's disease (AD). Oxidative stress in brain tissues is intimately related to AD. In this report, we examined oxidative stress status in cerebral cortex in 2-, 4- and 7-month PS cDKO and the age- and gender-matched control mice (WT). Lipid peroxidation (MDA as the measure) and protein oxidation (protein carbonyl as the measure) were found to be significantly increased in PS cDKO mice over the age points examined, notably in those at 2-month, suggesting that oxidative stress is an early event in response to PS loss-of-function. The oxidative modification of cortical proteins was further confirmed by Oxyblot assay. The investigations into endogenous antioxidant defense (CAT, SOD and GSH-px as measures) revealed a compensatory defense against oxidative stress, particularly at the early age stage, in PS cDKO mice. The expression level of cortical glial fibrillary acidic protein (GFAP) increased in an age-related manner, in particular in 2-month PS cDKO mice, suggesting that the interaction relationship between oxidative stress and inflammatory response may be closely associated with the underlying loss-of-function pathogenesis of AD.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Gu, F., Zhu, M., Shi, J., Hu, Y., & Zhao, Z. (2008). Enhanced oxidative stress is an early event during development of Alzheimer-like pathologies in presenilin conditional knock-out mice. Neuroscience letters. https://doi.org/10.1016/j.neulet.2008.05.050
Vancouver
Gu F, Zhu M, Shi J, Hu Y, Zhao Z. Enhanced oxidative stress is an early event during development of Alzheimer-like pathologies in presenilin conditional knock-out mice. Neuroscience letters. 2008. doi:10.1016/j.neulet.2008.05.050. PMID: 18539391.
BibTeX
@article{gu2008-18539391,
author = {Gu, F. and Zhu, M. and Shi, J. and Hu, Y. and Zhao, Z.},
title = {{Enhanced oxidative stress is an early event during development of Alzheimer-like pathologies in presenilin conditional knock-out mice}},
journal = {Neuroscience letters},
year = {2008},
doi = {10.1016/j.neulet.2008.05.050},
pmid = {18539391},
url = {https://doi.org/10.1016/j.neulet.2008.05.050}
}
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
- Lipid peroxidation (MDA as the measure) and protein oxidation (protein carbonyl as the measure) were found to be significantly increased in PS cDKO mice over the age points examined, notably in those at 2-month, suggesting that oxidative stress is an early event in response to PS loss-of-function.
- The investigations into endogenous antioxidant defense (CAT, SOD and GSH-px as measures) revealed a compensatory defense against oxidative stress, particularly at the early age stage, in PS cDKO mice.
- The expression level of cortical glial fibrillary acidic protein (GFAP) increased in an age-related manner, in particular in 2-month PS cDKO mice, suggesting that the interaction relationship between oxidative stress and inflammatory response may be closely associated with the underlying loss-of-function pathogenesis of AD.
Why it matters
In presenilin conditional knock-out mice, this study found increased markers of oxidative stress, notably at 2 months, suggesting oxidative stress is an early event after presenilin loss-of-function. It is an animal study and does not test any treatment, cure or prevention in people.
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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 randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Neuroscience letters) |
| Journal's citation record | 3 / 4 | Neuroscience Letters: journal h-index 267 (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 | 1 / 5 | 2008 — within 20 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 “mice”) — scores zero |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 4 / 7 | Cited 84 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 4.2 citations a year over 20 year(s) since 2008 |
| Impact for its field and year | 3 / 6 | Cited 4.6× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 1 other studies in this library |
| Still being cited | 1 / 4 | Cited 8 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Zheng Yan Zhao: h-index 21 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | East China Normal University: institution h-index 506 (OpenAlex) |
| Multi-centre 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 18539391) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 37 / 100 | — |
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