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c-Jun N-terminal kinase regulates soluble Aβ oligomers and cognitive impairment in AD mouse model
Sclip A, Antoniou X, Colombo A, Camici GG, Pozzi L, Cardinetti D, Feligioni M, Veglianese P et al.. The Journal of biological chemistry, 2011-10-27
Topic: Brain proteins, microglia and lab models
Alzheimer disease (AD) is characterized by cognitive impairment that starts with memory loss to end in dementia. Loss of synapses and synaptic dysfunction are closely associated with cognitive impairment in AD patients. Biochemical and pathological evidence suggests that soluble Aβ oligomers correlate with cognitive impairment. Here, we used the TgCRND8 AD mouse model to investigate the role of JNK in long term memory deficits. TgCRND8 mice were chronically treated with the cell-penetrating c-Jun N-terminal kinase inhibitor peptide (D-JNKI1). D-JNKI1, preventing JNK action, completely rescued memory impairments (behavioral studies) as well as the long term potentiation deficits of TgCRND8 mice. Moreover, D-JNKI1 inhibited APP phosphorylation in Thr-668 and reduced the amyloidogenic cleavage of APP and Aβ oligomers in brain parenchyma of treated mice. In conclusion, by regulating key pathogenic mechanisms of AD, JNK might hold promise as innovative therapeutic target.
Key findings
- Loss of synapses and synaptic dysfunction are closely associated with cognitive impairment in AD patients.
- Biochemical and pathological evidence suggests that soluble Aβ oligomers correlate with cognitive impairment.
- In conclusion, by regulating key pathogenic mechanisms of AD, JNK might hold promise as innovative therapeutic target.
Study details
- Evidence strengthLow
How this study scored 36/100
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. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 21 of the 58 points we could judge it on, which is 36 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (The Journal of biological chemistry) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| 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 | 2011 — within 20 year(s) of the newest study here |
| 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 | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 22033930) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 21 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 21 of the 58 points we could judge it on is 36 out of 100. |
| Total | 36 / 100 | — |
What each of these 20 components measures, and what this score is not →
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Cite this study APA, Vancouver, BibTeX · download .bib or .ris
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APA 7th
Sclip, A., Antoniou, X., Colombo, A., Camici, G. G., Pozzi, L., Cardinetti, D., et al. (2011). c-Jun N-terminal kinase regulates soluble Aβ oligomers and cognitive impairment in AD mouse model. The Journal of biological chemistry. https://doi.org/10.1074/jbc.m111.297515
Vancouver
Sclip A, Antoniou X, Colombo A, Camici GG, Pozzi L, Cardinetti D, et al. c-Jun N-terminal kinase regulates soluble Aβ oligomers and cognitive impairment in AD mouse model. The Journal of biological chemistry. 2011. doi:10.1074/jbc.m111.297515. PMID: 22033930.
BibTeX
@article{sclip2011-22033930,
author = {Sclip, A. and Antoniou, X. and Colombo, A. and Camici, G. G. and Pozzi, L. and Cardinetti, D. and Feligioni, M. and Veglianese, P. and others},
title = {{c-Jun N-terminal kinase regulates soluble Aβ oligomers and cognitive impairment in AD mouse model}},
journal = {The Journal of biological chemistry},
year = {2011},
doi = {10.1074/jbc.m111.297515},
pmid = {22033930},
url = {https://doi.org/10.1074/jbc.m111.297515}
}
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