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Amyloid fibrils activate tyrosine kinase-dependent signaling and superoxide production in microglia
McDonald DR, Brunden KR, Landreth GE.. The Journal of neuroscience : the official journal of the Society for Neuroscience, 1997-04-01
Topic: Brain proteins, microglia and lab models
Plain-language summary
Alzheimer's disease (AD) is a devastating neurological disorder characterized by loss of cognitive skills and progressive dementia. The pathological hallmark of AD is the presence of numerous senile plaques throughout the hippocampus and cerebral cortex associated with degenerating axons, neurofibrillary tangles, and gliosis. The core of the senile plaque primarily is composed of the 39-43 amino acid beta-amyloid peptide (Abeta), which forms fibrils of beta-pleated sheets.
What this study adds
Evidence grade: Low
This laboratory study describes how beta-amyloid fibrils activate signaling and superoxide production in microglia, but it states that a direct causal link between beta-amyloid and Alzheimer's disease remains to be established. It offers no treatment, cure or prevention.
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
McDonald, D. R., Brunden, K. R., & Landreth, G. E. (1997). Amyloid fibrils activate tyrosine kinase-dependent signaling and superoxide production in microglia. The Journal of neuroscience : the official journal of the Society for Neuroscience. https://doi.org/10.1523/jneurosci.17-07-02284.1997
Vancouver
McDonald DR, Brunden KR, Landreth GE. Amyloid fibrils activate tyrosine kinase-dependent signaling and superoxide production in microglia. The Journal of neuroscience : the official journal of the Society for Neuroscience. 1997. doi:10.1523/jneurosci.17-07-02284.1997. PMID: 9065490.
BibTeX
@article{mcdonald1997-9065490,
author = {McDonald, D. R. and Brunden, K. R. and Landreth, G. E.},
title = {{Amyloid fibrils activate tyrosine kinase-dependent signaling and superoxide production in microglia}},
journal = {The Journal of neuroscience : the official journal of the Society for Neuroscience},
year = {1997},
doi = {10.1523/jneurosci.17-07-02284.1997},
pmid = {9065490},
url = {https://doi.org/10.1523/jneurosci.17-07-02284.1997}
}
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
- The pathological hallmark of AD is the presence of numerous senile plaques throughout the hippocampus and cerebral cortex associated with degenerating axons, neurofibrillary tangles, and gliosis.
- The core of the senile plaque primarily is composed of the 39-43 amino acid beta-amyloid peptide (Abeta), which forms fibrils of beta-pleated sheets.
- Although considerable genetic evidence implicates Abeta in the pathogenesis of AD, a direct causal link remains to be established.
- Senile plaques are foci of local inflammatory processes, as evidenced by the presence of numerous activated microglia and acute phase proteins.
Why it matters
This laboratory study describes how beta-amyloid fibrils activate signaling and superoxide production in microglia, but it states that a direct causal link between beta-amyloid and Alzheimer's disease remains to be established. It offers no treatment, cure or prevention.
Study details
- Evidence strengthLow
How this study scored 47/100
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 (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 | 1997 — 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 317 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 10.2 citations a year over 31 year(s) since 1997 |
| Impact for its field and year | 4 / 6 | Cited 8.5× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 15 other studies in this library |
| Still being cited | 1 / 4 | Cited 6 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Gary E. Landreth: h-index 101 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Case Western Reserve University: institution h-index 1,159 (OpenAlex) |
| Multicenter collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 9065490) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 47 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1523/jneurosci.17-07-02284.1997
- PubMed: 9065490
- 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).
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