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This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Inflammation and the immune system

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

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

How this study scored 46/100
How this study's score is builtJournal tier 7 of 10; Journal's citation record 3 of 4; Study design 0 of 12; Strength of evidence 1 of 5; Peer-review validation 10 of 10; How recent 1 of 5; Sample size 0 of 4; Effect reported 0 of 3; Studied in people 0 of 3; Randomized / blinded 0 of 2; Times cited 6 of 7; Citations per year 3 of 5; Impact for its field and year 3 of 6; Cited by studies here 3 of 6; Still being cited 3 of 4; Senior author's track record 3 of 4; Institution's track record 0 of 3; Multicenter collaboration 1 of 3; Indexed in PubMed 2 of 2; Free to read 0 of 2. Total 46 of 100.46 of 100 points earned54 not earned

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.

ComponentPointsWhy
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

Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).

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