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Neuronal death induced by nanomolar amyloid β is mediated by primary phagocytosis of neurons by microglia
Neniskyte U, Neher JJ, Brown GC.. The Journal of biological chemistry, 2011-09-08
Topic: Brain proteins, microglia and lab models
Alzheimer disease is characterized by neuronal loss and brain plaques of extracellular amyloid β (Aβ), but the means by which Aβ may induce neuronal loss is not entirely clear. Although high concentrations of Aβ (μM) can induce direct toxicity to neurons, we find that low concentration (nM) induce neuronal loss through a microglia-mediated mechanism. In mixed neuronal-glial cultures from rat cerebellum, 250 nM Aβ1-42 (added as monomers, oligomers or fibers) induced about 30% loss of neurons between 2 and 3 days.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Neniskyte, U., Neher, J. J., & Brown, G. C. (2011). Neuronal death induced by nanomolar amyloid β is mediated by primary phagocytosis of neurons by microglia. The Journal of biological chemistry. https://doi.org/10.1074/jbc.m111.267583
Vancouver
Neniskyte U, Neher JJ, Brown GC. Neuronal death induced by nanomolar amyloid β is mediated by primary phagocytosis of neurons by microglia. The Journal of biological chemistry. 2011. doi:10.1074/jbc.m111.267583. PMID: 21903584.
BibTeX
@article{neniskyte2011-21903584,
author = {Neniskyte, U. and Neher, J. J. and Brown, G. C.},
title = {{Neuronal death induced by nanomolar amyloid β is mediated by primary phagocytosis of neurons by microglia}},
journal = {The Journal of biological chemistry},
year = {2011},
doi = {10.1074/jbc.m111.267583},
pmid = {21903584},
url = {https://doi.org/10.1074/jbc.m111.267583}
}
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
- Although high concentrations of Aβ (μM) can induce direct toxicity to neurons, we find that low concentration (nM) induce neuronal loss through a microglia-mediated mechanism.
- In mixed neuronal-glial cultures from rat cerebellum, 250 nM Aβ1-42 (added as monomers, oligomers or fibers) induced about 30% loss of neurons between 2 and 3 days.
- This neuronal loss occurred without any increase in neuronal apoptosis or necrosis, and no neuronal loss occurred with Aβ42-1.
- Aβ greatly increased the phagocytic capacity of microglia and induced phosphatidylserine exposure (an "eat-me" signal) on neuronal processes.
Why it matters
In rat cell cultures, low concentrations of amyloid beta caused neurons to be lost through a process in which microglia engulfed them, rather than through direct toxicity or classic cell death. This is laboratory work in cells, so it is early and does not establish a treatment or prevention approach for patients.
Study details
- Evidence strengthLow
How this study scored 48/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (The Journal of biological chemistry) |
| Journal's citation record | 4 / 4 | Journal of Biological Chemistry: journal h-index 780 (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 | 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 | 5 / 7 | Cited 209 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 12.3 citations a year over 17 year(s) since 2011 |
| Impact for its field and year | 4 / 6 | Cited 9.3× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 4 other studies in this library |
| Still being cited | 2 / 4 | Cited 32 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Guy Charles Brown: h-index 88 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of Cambridge: institution h-index 1,973 (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 21903584) |
| Free to read | 2 / 2 | Free to read |
| Total | 48 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1074/jbc.m111.267583
- PubMed: 21903584
- Original source →
- Free full text: Journal of Biological Chemistry →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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