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Interleukin-6 induces Alzheimer-type phosphorylation of tau protein by deregulating the cdk5/p35 pathway
Quintanilla RA, Orellana DI, González-Billault C, Maccioni RB.. Experimental cell research, 2004-04-01
Topic: Brain proteins, microglia and lab models
Plain-language summary
Inflammation is a process that has been actively related with the onset of several neurodegenerative disorders including Alzheimer disease (AD). However, the precise implications of inflammatory response for neurodegeneration have not been elucidated. A current hypothesis considers that extracellular insults to neurons could trigger the production of inflammatory cytokines by astrocytes and microglia.
What this study adds
Evidence grade: Low
This laboratory study describes how the inflammatory cytokine interleukin-6 can lead to Alzheimer-type phosphorylation of tau protein by disrupting the cdk5/p35 pathway. It is early mechanistic work and does not show that blocking this process treats or prevents Alzheimer's disease in people.
Taken from this record’s own fields, not from reading the paper. The grade is assigned from the abstract’s wording; what that means.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Quintanilla, R. A., Orellana, D. I., González-Billault, C., & Maccioni, R. B. (2004). Interleukin-6 induces Alzheimer-type phosphorylation of tau protein by deregulating the cdk5/p35 pathway. Experimental cell research. https://doi.org/10.1016/j.yexcr.2004.01.002
Vancouver
Quintanilla RA, Orellana DI, González-Billault C, Maccioni RB. Interleukin-6 induces Alzheimer-type phosphorylation of tau protein by deregulating the cdk5/p35 pathway. Experimental cell research. 2004. doi:10.1016/j.yexcr.2004.01.002. PMID: 15051507.
BibTeX
@article{quintanilla2004-15051507,
author = {Quintanilla, R. A. and Orellana, D. I. and González-Billault, C. and Maccioni, R. B.},
title = {{Interleukin-6 induces Alzheimer-type phosphorylation of tau protein by deregulating the cdk5/p35 pathway}},
journal = {Experimental cell research},
year = {2004},
doi = {10.1016/j.yexcr.2004.01.002},
pmid = {15051507},
url = {https://doi.org/10.1016/j.yexcr.2004.01.002}
}
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
- However, the precise implications of inflammatory response for neurodegeneration have not been elucidated.
- A current hypothesis considers that extracellular insults to neurons could trigger the production of inflammatory cytokines by astrocytes and microglia.
- These cytokines, namely, interleukin (IL)-1beta, TNFalpha, and IL-6, could affect the normal behavior of neuronal cells.
- In the present study, we describe the effect of the administration at physiologic doses of one of these cytokines, IL-6, to hippocampal neurons, on the protein kinase pathways as well as on the tau phosphorylation patterns.
Why it matters
This laboratory study describes how the inflammatory cytokine interleukin-6 can lead to Alzheimer-type phosphorylation of tau protein by disrupting the cdk5/p35 pathway. It is early mechanistic work and does not show that blocking this process treats or prevents Alzheimer's disease in people.
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 randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Experimental cell research) |
| Journal's citation record | 3 / 4 | Experimental Cell Research: journal h-index 284 (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 | 2004 — older than 20 years, still counted |
| 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) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 6 / 7 | Cited 453 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 18.9 citations a year over 24 year(s) since 2004 |
| Impact for its field and year | 3 / 6 | Cited 5.3× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 19 other studies in this library |
| Still being cited | 3 / 4 | Cited 87 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Ricardo Benjamin Maccioni: h-index 54 (OpenAlex, whole career) |
| Institution's track record | 0 / 3 | University of Chile: institution h-index 541 (OpenAlex) |
| Multicenter collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 15051507) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 46 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1016/j.yexcr.2004.01.002
- PubMed: 15051507
- Original source →
- Free full text: Americanae (AECID Library) →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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