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A1 adenosine receptors accumulate in neurodegenerative structures in Alzheimer disease and mediate both amyloid precursor protein processing and tau phosphorylation and translocation
Angulo E, Casadó V, Mallol J, Canela EI, Viñals F, Ferrer I, Lluis C, Franco R.. Brain pathology (Zurich, Switzerland), 2003-10-01
Topic: Brain proteins, microglia and lab models
Immunostaining of adenosine receptors in the hippocampus and cerebral cortex from necropsies of Alzheimer disease (AD) patients shows that there is a change in the pattern of expression and a redistribution of receptors in these brain areas when compared with samples from controls. Adenosine A1 receptor (A1R) immunoreactivity was found in degenerating neurons with neurofibrillary tangles and in dystrophic neurites of senile plaques. A high degree of colocalization for A1R and betaA4 amyloid in senile plaques and for A1R and tau in neurons with tau deposition, but without tangles, was seen.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Angulo, E., Casadó, V., Mallol, J., Canela, E. I., Viñals, F., Ferrer, I., et al. (2003). A1 adenosine receptors accumulate in neurodegenerative structures in Alzheimer disease and mediate both amyloid precursor protein processing and tau phosphorylation and translocation. Brain pathology (Zurich, Switzerland). https://doi.org/10.1111/j.1750-3639.2003.tb00475.x
Vancouver
Angulo E, Casadó V, Mallol J, Canela EI, Viñals F, Ferrer I, et al. A1 adenosine receptors accumulate in neurodegenerative structures in Alzheimer disease and mediate both amyloid precursor protein processing and tau phosphorylation and translocation. Brain pathology (Zurich, Switzerland). 2003. doi:10.1111/j.1750-3639.2003.tb00475.x. PMID: 14655750.
BibTeX
@article{angulo2003-14655750,
author = {Angulo, E. and Casadó, V. and Mallol, J. and Canela, E. I. and Viñals, F. and Ferrer, I. and Lluis, C. and Franco, R.},
title = {{A1 adenosine receptors accumulate in neurodegenerative structures in Alzheimer disease and mediate both amyloid precursor protein processing and tau phosphorylation and translocation}},
journal = {Brain pathology (Zurich, Switzerland)},
year = {2003},
doi = {10.1111/j.1750-3639.2003.tb00475.x},
pmid = {14655750},
url = {https://doi.org/10.1111/j.1750-3639.2003.tb00475.x}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record names 8 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
Key findings
- Adenosine A1 receptor (A1R) immunoreactivity was found in degenerating neurons with neurofibrillary tangles and in dystrophic neurites of senile plaques.
- A high degree of colocalization for A1R and betaA4 amyloid in senile plaques and for A1R and tau in neurons with tau deposition, but without tangles, was seen.
- Additionally, adenosine A2A receptors, located mainly in striatal neurons in controls, appeared in glial cells in the hippocampus and cerebral cortex of patients.
- On comparing similar samples from controls and patients, no significant change was evident for metabotropic glutamate receptors.
Why it matters
This study found adenosine A1 receptors in degenerating neurons with tangles and in the dystrophic neurites of senile plaques in Alzheimer's brain tissue, and A2A receptors appeared in glial cells. It describes where these receptors are located in diseased brain but does not test any treatment, cure or prevention.
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Study details
- Evidence strengthLow
How this study scored 39/100
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 (Brain pathology (Zurich, Switzerland)) |
| Journal's citation record | 2 / 4 | Brain Pathology: journal h-index 183 (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 | 5 / 7 | Cited 178 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 7.1 citations a year over 25 year(s) since 2003 |
| Impact for its field and year | 2 / 6 | Cited 2.5× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 2 other studies in this library |
| Still being cited | 2 / 4 | Cited 21 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Rafael Franco: h-index 93 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Universitat de Barcelona: institution h-index 1,049 (OpenAlex) |
| Multi-centre 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 14655750) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 39 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1111/j.1750-3639.2003.tb00475.x
- PubMed: 14655750
- Original source →
- Free full text: PubMed Central →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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