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Activation of microglia by amyloid {beta} requires P2X7 receptor expression
Sanz JM, Chiozzi P, Ferrari D, Colaianna M, Idzko M, Falzoni S, Fellin R, Trabace L et al.. Journal of immunology (Baltimore, Md. : 1950), 2009-04-01
Topic: Brain proteins, microglia and lab models
Extracellular ATP is a mediator of intercellular communication and a danger signal. Release of this and other nucleotides modulates microglia responses via P2Y and P2X receptors, among which the P2X(7) subtype stands out for its proinflammatory activity and for up-regulation in a transgenic model of Alzheimer disease and in brains from Alzheimer disease patients. Here we show that amyloid beta (Abeta) triggered increases in intracellular Ca(2+) ([Ca(2+)](i)), ATP release, IL-1beta secretion, and plasma membrane permeabilization in microglia from wild-type but not from P2X(7)-deleted mice.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Sanz, J. M., Chiozzi, P., Ferrari, D., Colaianna, M., Idzko, M., Falzoni, S., et al. (2009). Activation of microglia by amyloid {beta} requires P2X7 receptor expression. Journal of immunology (Baltimore, Md. : 1950). https://doi.org/10.4049/jimmunol.0803612
Vancouver
Sanz JM, Chiozzi P, Ferrari D, Colaianna M, Idzko M, Falzoni S, et al. Activation of microglia by amyloid {beta} requires P2X7 receptor expression. Journal of immunology (Baltimore, Md. : 1950). 2009. doi:10.4049/jimmunol.0803612. PMID: 19299738.
BibTeX
@article{sanz2009-19299738,
author = {Sanz, J. M. and Chiozzi, P. and Ferrari, D. and Colaianna, M. and Idzko, M. and Falzoni, S. and Fellin, R. and Trabace, L. and others},
title = {{Activation of microglia by amyloid beta requires P2X7 receptor expression}},
journal = {Journal of immunology (Baltimore, Md. : 1950)},
year = {2009},
doi = {10.4049/jimmunol.0803612},
pmid = {19299738},
url = {https://doi.org/10.4049/jimmunol.0803612}
}
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Key findings
- Release of this and other nucleotides modulates microglia responses via P2Y and P2X receptors, among which the P2X(7) subtype stands out for its proinflammatory activity and for up-regulation in a transgenic model of Alzheimer disease and in brains from Alzheimer disease patients.
- Here we show that amyloid beta (Abeta) triggered increases in intracellular Ca(2+) ([Ca(2+)](i)), ATP release, IL-1beta secretion, and plasma membrane permeabilization in microglia from wild-type but not from P2X(7)-deleted mice.
- Likewise, intra-hippocampal injection of Abeta caused a large accumulation of IL-1beta in wild-type but not in P2X(7)(-/-) mice.
- These observations suggest that Abeta activates a purinergic autocrine/paracrine stimulatory loop of which the P2X(7) receptor is an obligate component.
Why it matters
In microglia from mice, amyloid beta triggered calcium increases, ATP release, IL-1beta secretion and membrane permeabilization only when the P2X7 receptor was present. This is laboratory animal and cell research, not a treatment or cure for Alzheimer's disease.
Study details
- Evidence strengthLow
How this study scored 46/100
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 (Journal of immunology (Baltimore, Md. : 1950)) |
| Journal's citation record | 4 / 4 | The Journal of Immunology: journal h-index 531 (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 | 2009 — 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 293 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 15.4 citations a year over 19 year(s) since 2009 |
| Impact for its field and year | 4 / 6 | Cited 8.4× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 5 other studies in this library |
| Still being cited | 2 / 4 | Cited 47 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Francesco Di Virgilio: h-index 115 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | University Medical Center Freiburg: institution h-index 675 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 19299738) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 46 / 100 | — |
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