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Brain oligomeric β-amyloid but not total amyloid plaque burden correlates with neuronal loss and astrocyte inflammatory response in amyloid precursor protein/tau transgenic mice
DaRocha-Souto B, Scotton TC, Coma M, Serrano-Pozo A, Hashimoto T, Serenó L, Rodríguez M, Sánchez B et al.. Journal of neuropathology and experimental neurology, 2011-05-01
Topic: Brain proteins, microglia and lab models
It has long been assumed that β-amyloid (Aβ) had to assemble into fibrillar amyloid plaques to exert its neurotoxic effects in Alzheimer disease. An alternative hypothesis is that soluble oligomers ofAβ play a much larger role in neuronal damage than the insoluble component. We have tested these competing hypotheses in vivo by studying the clinicopathologic correlates of oligomeric Aβ species and classic fibrillar amyloid plaques in the brains of double-transgenic APP-tau mice up to 17 months of age.
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APA 7th
DaRocha-Souto, B., Scotton, T. C., Coma, M., Serrano-Pozo, A., Hashimoto, T., Serenó, L., et al. (2011). Brain oligomeric β-amyloid but not total amyloid plaque burden correlates with neuronal loss and astrocyte inflammatory response in amyloid precursor protein/tau transgenic mice. Journal of neuropathology and experimental neurology. https://doi.org/10.1097/nen.0b013e318217a118
Vancouver
DaRocha-Souto B, Scotton TC, Coma M, Serrano-Pozo A, Hashimoto T, Serenó L, et al. Brain oligomeric β-amyloid but not total amyloid plaque burden correlates with neuronal loss and astrocyte inflammatory response in amyloid precursor protein/tau transgenic mice. Journal of neuropathology and experimental neurology. 2011. doi:10.1097/nen.0b013e318217a118. PMID: 21487307.
BibTeX
@article{darochasouto2011-21487307,
author = {DaRocha-Souto, B. and Scotton, T. C. and Coma, M. and Serrano-Pozo, A. and Hashimoto, T. and Serenó, L. and Rodríguez, M. and Sánchez, B. and others},
title = {{Brain oligomeric β-amyloid but not total amyloid plaque burden correlates with neuronal loss and astrocyte inflammatory response in amyloid precursor protein/tau transgenic mice}},
journal = {Journal of neuropathology and experimental neurology},
year = {2011},
doi = {10.1097/nen.0b013e318217a118},
pmid = {21487307},
url = {https://doi.org/10.1097/nen.0b013e318217a118}
}
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
- An alternative hypothesis is that soluble oligomers ofAβ play a much larger role in neuronal damage than the insoluble component.
- We have tested these competing hypotheses in vivo by studying the clinicopathologic correlates of oligomeric Aβ species and classic fibrillar amyloid plaques in the brains of double-transgenic APP-tau mice up to 17 months of age.
- Biochemical and immunohistochemical measures of brain oligomeric Aβ exponentially increased with age.
- Oligomeric Aβ load correlated with morphological markers of fibrillar Aβ deposition.
Why it matters
In double-transgenic APP-tau mice, brain oligomeric amyloid-beta but not total plaque burden correlated with neuronal loss and astrocyte inflammatory response. This is animal evidence about which form of amyloid-beta relates to damage and does not test a treatment in people.
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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 and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Journal of neuropathology and experimental neurology) |
| Journal's citation record | 2 / 4 | Journal of Neuropathology & Experimental Neurology: journal h-index 239 (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 | 2011 — 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 “transgenic”) — scores zero |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 126 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 7.4 citations a year over 17 year(s) since 2011 |
| 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 | 2 / 6 | Cited by 9 other studies in this library |
| Still being cited | 2 / 4 | Cited 16 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Teresa Gómez‐Isla: h-index 66 (OpenAlex, whole career) |
| Institution's track record | 3 / 3 | Harvard University: institution h-index 3,235 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 4 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 21487307) |
| 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 →
Read the original
- DOI: 10.1097/nen.0b013e318217a118
- PubMed: 21487307
- Original source →
- Free full text: Journal of Neuropathology & Experimental Neurology →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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