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Interleukin-1 mediates pathological effects of microglia on tau phosphorylation and on synaptophysin synthesis in cortical neurons through a p38-MAPK pathway
Li Y, Liu L, Barger SW, Griffin WS.. The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003-03-01
Topic: Brain proteins, microglia and lab models
The presence of tangles of abnormally phosphorylated tau is a characteristic of Alzheimer's disease (AD), and the loss of synapses correlates with the degree of dementia. In addition, the overexpression of interleukin-1 (IL-1) has been implicated in tangle formation in AD. As a direct test of the requirement for IL-1 in tau phosphorylation and synaptophysin expression, IL-1 actions in neuron-microglia cocultures were manipulated.
Key findings
- In addition, the overexpression of interleukin-1 (IL-1) has been implicated in tangle formation in AD.
- As a direct test of the requirement for IL-1 in tau phosphorylation and synaptophysin expression, IL-1 actions in neuron-microglia cocultures were manipulated.
- Activation of microglia with secreted beta-amyloid precursor protein or lipopolysaccharide elevated their expression of IL-1alpha, IL-1beta, and tumor necrosis factor alpha (TNFalpha) mRNA.
- When such activated microglia were placed in coculture with primary neocortical neurons, a significant increase in the phosphorylation of neuronal tau was accompanied by a decline in synaptophysin levels.
Why it matters
In a laboratory experiment using microglia and neurons grown together in a dish, microglia activated with secreted beta-amyloid precursor protein or lipopolysaccharide made more IL-1 and TNFα mRNA. When these microglia were placed with neurons, the study reports "a significant increase in the phosphorylation of neuronal tau … accompanied by a decline in synaptophysin levels," and its title attributes these effects to interleukin-1. This is cell-culture work only: it reports no treatment, cure or prevention.
Study details
- Evidence strengthLow
How this study scored 51/100
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 neuroscience : the official journal of the Society for Neuroscience) |
| Journal's citation record | 4 / 4 | Journal of Neuroscience: journal h-index 651 (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 | 2003 — 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) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 6 / 7 | Cited 561 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 22.4 citations a year over 25 year(s) since 2003 |
| Impact for its field and year | 4 / 6 | Cited 10.5× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 4 / 6 | Cited by 39 other studies in this library |
| Still being cited | 3 / 4 | Cited 64 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author W. Sue T. Griffin: h-index 66 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Veterans Health Administration: institution h-index 968 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 12629164) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 51 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1523/jneurosci.23-05-01605.2003
- PubMed: 12629164
- Original source →
- Free full text: Journal of Neuroscience →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
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.
APA 7th
Li, Y., Liu, L., Barger, S. W., & Griffin, W. S. (2003). Interleukin-1 mediates pathological effects of microglia on tau phosphorylation and on synaptophysin synthesis in cortical neurons through a p38-MAPK pathway. The Journal of neuroscience : the official journal of the Society for Neuroscience. https://doi.org/10.1523/jneurosci.23-05-01605.2003
Vancouver
Li Y, Liu L, Barger SW, Griffin WS. Interleukin-1 mediates pathological effects of microglia on tau phosphorylation and on synaptophysin synthesis in cortical neurons through a p38-MAPK pathway. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2003. doi:10.1523/jneurosci.23-05-01605.2003. PMID: 12629164.
BibTeX
@article{li2003-12629164,
author = {Li, Y. and Liu, L. and Barger, S. W. and Griffin, W. S.},
title = {{Interleukin-1 mediates pathological effects of microglia on tau phosphorylation and on synaptophysin synthesis in cortical neurons through a p38-MAPK pathway}},
journal = {The Journal of neuroscience : the official journal of the Society for Neuroscience},
year = {2003},
doi = {10.1523/jneurosci.23-05-01605.2003},
pmid = {12629164},
url = {https://doi.org/10.1523/jneurosci.23-05-01605.2003}
}
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