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Phagocytosis executes delayed neuronal death after focal brain ischemia
Neher JJ, Emmrich JV, Fricker M, Mander PK, Théry C, Brown GC.. Proceedings of the National Academy of Sciences of the United States of America, 2013-10-07
Topic: Brain proteins, microglia and lab models
Delayed neuronal loss and brain atrophy after cerebral ischemia contribute to stroke and dementia pathology, but the mechanisms are poorly understood. Phagocytic removal of neurons is generally assumed to be beneficial and to occur only after neuronal death. However, we report herein that inhibition of phagocytosis can prevent delayed loss and death of functional neurons after transient brain ischemia.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Neher, J. J., Emmrich, J. V., Fricker, M., Mander, P. K., Théry, C., & Brown, G. C. (2013). Phagocytosis executes delayed neuronal death after focal brain ischemia. Proceedings of the National Academy of Sciences of the United States of America. https://doi.org/10.1073/pnas.1308679110
Vancouver
Neher JJ, Emmrich JV, Fricker M, Mander PK, Théry C, Brown GC. Phagocytosis executes delayed neuronal death after focal brain ischemia. Proceedings of the National Academy of Sciences of the United States of America. 2013. doi:10.1073/pnas.1308679110. PMID: 24101459.
BibTeX
@article{neher2013-24101459,
author = {Neher, J. J. and Emmrich, J. V. and Fricker, M. and Mander, P. K. and Théry, C. and Brown, G. C.},
title = {{Phagocytosis executes delayed neuronal death after focal brain ischemia}},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
year = {2013},
doi = {10.1073/pnas.1308679110},
pmid = {24101459},
url = {https://doi.org/10.1073/pnas.1308679110}
}
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
- Phagocytic removal of neurons is generally assumed to be beneficial and to occur only after neuronal death.
- However, we report herein that inhibition of phagocytosis can prevent delayed loss and death of functional neurons after transient brain ischemia.
- Two phagocytic proteins, Mer receptor tyrosine kinase (MerTK) and Milk fat globule EGF-like factor 8 (MFG-E8), were transiently up-regulated by macrophages/microglia after focal brain ischemia in vivo.
- Strikingly, deficiency in either protein completely prevented long-term functional motor deficits after cerebral ischemia and strongly reduced brain atrophy as a result of inhibiting phagocytosis of neurons.
Why it matters
In this study, blocking phagocytosis prevented delayed loss and death of functional neurons after transient brain ischemia in mice, and deficiency in either of two phagocytic proteins was protective. This is animal research on stroke-related neuronal death, not a demonstrated Alzheimer's treatment.
Study details
- Evidence strengthLow
How this study scored 50/100
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 (Proceedings of the National Academy of Sciences of the United States of America) |
| Journal's citation record | 4 / 4 | Proceedings of the National Academy of Sciences: journal h-index 1,167 (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 | 2013 — 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 | 6 / 7 | Cited 353 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 23.5 citations a year over 15 year(s) since 2013 |
| Impact for its field and year | 4 / 6 | Cited 10.8× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 2 other studies in this library |
| Still being cited | 3 / 4 | Cited 78 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 | Inserm: institution h-index 1,988 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 5 institution(s) in 3 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 24101459) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 50 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1073/pnas.1308679110
- PubMed: 24101459
- Original source →
- Free full text: Proceedings of the National Academy of Sciences →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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