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Severe reactive astrocytes precipitate pathological hallmarks of Alzheimer's disease via H2O2- production
Chun H, Im H, Kang YJ, Kim Y, Shin JH, Won W, Lim J, Ju Y et al.. Nature neuroscience, 2020-11-16
Topic: Amyloid, tau and blood-test diagnosis
Although the pathological contributions of reactive astrocytes have been implicated in Alzheimer's disease (AD), their in vivo functions remain elusive due to the lack of appropriate experimental models and precise molecular mechanisms. Here, we show the importance of astrocytic reactivity on the pathogenesis of AD using GiD, a newly developed animal model of reactive astrocytes, where the reactivity of astrocytes can be manipulated as mild (GiDm) or severe (GiDs). Mechanistically, excessive hydrogen peroxide (H 2 O 2 ) originated from monoamine oxidase B in severe reactive astrocytes causes glial activation, tauopathy, neuronal death, brain atrophy, cognitive impairment and eventual death, which are significantly prevented by AAD-2004, a potent H 2 O 2 scavenger. These H 2 O 2 - -induced pathological features of AD in GiDs are consistently recapitulated in a three-dimensional culture AD model, virus-infected APP/PS1 mice and the brains of patients with AD. Our study identifies H 2 O 2 from severe but not mild reactive astrocytes as a key determinant of neurodegeneration in AD.
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APA 7th
Chun, H., Im, H., Kang, Y. J., Kim, Y., Shin, J. H., Won, W., et al. (2020). Severe reactive astrocytes precipitate pathological hallmarks of Alzheimer's disease via H2O2- production. Nature neuroscience. https://doi.org/10.1038/s41593-020-00735-y
Vancouver
Chun H, Im H, Kang YJ, Kim Y, Shin JH, Won W, et al. Severe reactive astrocytes precipitate pathological hallmarks of Alzheimer's disease via H2O2- production. Nature neuroscience. 2020. doi:10.1038/s41593-020-00735-y. PMID: 33199896.
BibTeX
@article{chun2020-33199896,
author = {Chun, H. and Im, H. and Kang, Y. J. and Kim, Y. and Shin, J. H. and Won, W. and Lim, J. and Ju, Y. and others},
title = {{Severe reactive astrocytes precipitate pathological hallmarks of Alzheimer's disease via H2O2- production}},
journal = {Nature neuroscience},
year = {2020},
doi = {10.1038/s41593-020-00735-y},
pmid = {33199896},
url = {https://doi.org/10.1038/s41593-020-00735-y}
}
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Key findings
- Mechanistically, excessive hydrogen peroxide (H 2 O 2 ) originated from monoamine oxidase B in severe reactive astrocytes causes glial activation, tauopathy, neuronal death, brain atrophy, cognitive impairment and eventual death, which are significantly prevented by AAD-2004, a potent H 2 O 2 scavenger.
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Study details
- Evidence strengthLow
How this study scored 41/100
Published in a leading specialty journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / 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 multi-centre collaboration, so those were left out: it earned 24 of the 58 points we could judge it on, which is 41 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (Nature neuroscience) |
| 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 | 2 / 5 | 2020 — within 10 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) |
| Randomised / blinded | 0 / 2 | No randomisation 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 |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 33199896) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 24 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 24 of the 58 points we could judge it on is 41 out of 100. |
| Total | 41 / 100 | — |
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