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NADPH oxidases: novel therapeutic targets for neurodegenerative diseases
Gao HM, Zhou H, Hong JS.. Trends in pharmacological sciences, 2012-04-11
Topic: Brain proteins, microglia and lab models
Plain-language summary
Oxidative stress is a key pathologic factor in neurodegenerative diseases such as Alzheimer and Parkinson diseases (AD, PD). The failure of free-radical-scavenging antioxidants in clinical trials pinpoints an urgent need to identify and to block major sources of oxidative stress in neurodegenerative diseases. As a major superoxide-producing enzyme complex in activated phagocytes, phagocyte NADPH oxidase (PHOX) is essential for host defense.
What this study adds
Evidence grade: Low
This is a narrative review. This review argues that overactivated phagocyte NADPH oxidase contributes to chronic neuroinflammation and neurodegeneration, and that blocking it might be a therapeutic target. It is based on preclinical evidence, so no NADPH oxidase treatment has been shown to work in people with Alzheimer's disease.
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
Gao, H. M., Zhou, H., & Hong, J. S. (2012). NADPH oxidases: novel therapeutic targets for neurodegenerative diseases. Trends in pharmacological sciences. https://doi.org/10.1016/j.tips.2012.03.008
Vancouver
Gao HM, Zhou H, Hong JS. NADPH oxidases: novel therapeutic targets for neurodegenerative diseases. Trends in pharmacological sciences. 2012. doi:10.1016/j.tips.2012.03.008. PMID: 22503440.
BibTeX
@article{gao2012-22503440,
author = {Gao, H. M. and Zhou, H. and Hong, J. S.},
title = {{NADPH oxidases: novel therapeutic targets for neurodegenerative diseases}},
journal = {Trends in pharmacological sciences},
year = {2012},
doi = {10.1016/j.tips.2012.03.008},
pmid = {22503440},
url = {https://doi.org/10.1016/j.tips.2012.03.008}
}
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 failure of free-radical-scavenging antioxidants in clinical trials pinpoints an urgent need to identify and to block major sources of oxidative stress in neurodegenerative diseases.
- As a major superoxide-producing enzyme complex in activated phagocytes, phagocyte NADPH oxidase (PHOX) is essential for host defense.
- However, recent preclinical evidence has underscored a pivotal role of overactivated PHOX in chronic neuroinflammation and progressive neurodegeneration.
- Deficiency in PHOX subunits mitigates neuronal damage induced by diverse insults/stresses relevant to neurodegenerative diseases.
Why it matters
This review argues that overactivated phagocyte NADPH oxidase contributes to chronic neuroinflammation and neurodegeneration, and that blocking it might be a therapeutic target. It is based on preclinical evidence, so no NADPH oxidase treatment has been shown to work in people with Alzheimer's disease.
Study details
- Evidence strengthLow
How this study scored 45/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Trends in pharmacological sciences) |
| Journal's citation record | 3 / 4 | Trends in Pharmacological Sciences: journal h-index 320 (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 | 2012 — 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 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 213 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 13.3 citations a year over 16 year(s) since 2012 |
| Impact for its field and year | 2 / 6 | Cited 1.2× 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 | 2 / 4 | Cited 30 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Jau‐Shyong Hong: h-index 101 (OpenAlex, whole career) |
| Institution's track record | 3 / 3 | National Institutes of Health: institution h-index 2,723 (OpenAlex) |
| Multicenter collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 22503440) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 45 / 100 | — |
What each of these 20 components measures, and what this score is not →
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