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Persistent improvement in synaptic and cognitive functions in an Alzheimer mouse model after rolipram treatment
Gong B, Vitolo OV, Trinchese F, Liu S, Shelanski M, Arancio O.. The Journal of clinical investigation, 2004-12-01
Topic: Brain proteins, microglia and lab models
Evidence suggests that Alzheimer disease (AD) begins as a disorder of synaptic function, caused in part by increased levels of amyloid beta-peptide 1-42 (Abeta42). Both synaptic and cognitive deficits are reproduced in mice double transgenic for amyloid precursor protein (AA substitution K670N,M671L) and presenilin-1 (AA substitution M146V). Here we demonstrate that brief treatment with the phosphodiesterase 4 inhibitor rolipram ameliorates deficits in both long-term potentiation (LTP) and contextual learning in the double-transgenic mice.
Key findings
- Both synaptic and cognitive deficits are reproduced in mice double transgenic for amyloid precursor protein (AA substitution K670N,M671L) and presenilin-1 (AA substitution M146V).
- Here we demonstrate that brief treatment with the phosphodiesterase 4 inhibitor rolipram ameliorates deficits in both long-term potentiation (LTP) and contextual learning in the double-transgenic mice.
- Most importantly, this beneficial effect can be extended beyond the duration of the administration.
- One course of long-term systemic treatment with rolipram improves LTP and basal synaptic transmission as well as working, reference, and associative memory deficits for at least 2 months after the end of the treatment.
Why it matters
In a mouse model, brief treatment with the phosphodiesterase 4 inhibitor rolipram improved synaptic and cognitive deficits, and the benefit lasted beyond the treatment period. This is an animal study, so it does not establish rolipram as a treatment, cure, or prevention for Alzheimer's disease in humans.
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Study details
- Evidence strengthLow
How this study scored 48/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported 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 clinical investigation) |
| Journal's citation record | 4 / 4 | Journal of Clinical Investigation: journal h-index 706 (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 | Laboratory or animal study (title names “mouse”) — scores zero |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 6 / 7 | Cited 434 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 18.1 citations a year over 24 year(s) since 2004 |
| Impact for its field and year | 4 / 6 | Cited 11.3× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 7 other studies in this library |
| Still being cited | 2 / 4 | Cited 37 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Ottavio Arancio: h-index 85 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | Columbia University: institution h-index 1,824 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 15578094) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 48 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1172/jci22831
- PubMed: 15578094
- Original source →
- Free full text: Journal of Clinical Investigation →
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
Gong, B., Vitolo, O. V., Trinchese, F., Liu, S., Shelanski, M., & Arancio, O. (2004). Persistent improvement in synaptic and cognitive functions in an Alzheimer mouse model after rolipram treatment. The Journal of clinical investigation. https://doi.org/10.1172/jci22831
Vancouver
Gong B, Vitolo OV, Trinchese F, Liu S, Shelanski M, Arancio O. Persistent improvement in synaptic and cognitive functions in an Alzheimer mouse model after rolipram treatment. The Journal of clinical investigation. 2004. doi:10.1172/jci22831. PMID: 15578094.
BibTeX
@article{gong2004-15578094,
author = {Gong, B. and Vitolo, O. V. and Trinchese, F. and Liu, S. and Shelanski, M. and Arancio, O.},
title = {{Persistent improvement in synaptic and cognitive functions in an Alzheimer mouse model after rolipram treatment}},
journal = {The Journal of clinical investigation},
year = {2004},
doi = {10.1172/jci22831},
pmid = {15578094},
url = {https://doi.org/10.1172/jci22831}
}
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