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Increased MYD88 blood transcript in a mouse model of Alzheimer's disease
Cucos CA, Dobre M, Dragnea EM, Manda G, Milanesi E.. BMC neuroscience, 2022-03-11
Topic: Amyloid, tau and blood-test diagnosis
Background Neuroinflammation plays a prominent role in Alzheimer's disease (AD), both in pathogenesis and disease progression. It has been shown that TLR/MYD88 signaling is involved in the chronic low-grade sterile inflammation associated with AD. Several studies have evidenced high levels of MYD88 in the brain of patients and animal models of AD, but no study has assessed so far its levels in blood. Methods In this study we evaluated the blood mRNA levels of MYD88 in a mouse model of AD, and also the putative effect of Rivastigmine treatment on MYD88 expression. Twenty-eight transgenic APP/TAU mice (AT) and twenty-two control C57/BL6j mice (WT) were included in this study, out of which five transgenic AT and five WT mice were treated with Rivastigmine. Results Increased MYD88 transcript in the whole blood from AT mice as compared to WT controls was found, which seems to increase in time due to disease progression and not to aging. This finding suggests that blood leukocytes are primed to develop TLR/MYD-mediated inflammatory processes. Moreover, results indicate that MYD88 blood levels were not modulated by the diseases-specific treatment with Rivastigmine. Conclusions Our results suggest that MYD88 might be a promising blood biomarker to monitor AD progression.
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APA 7th
Cucos, C. A., Dobre, M., Dragnea, E. M., Manda, G., & Milanesi, E. (2022). Increased MYD88 blood transcript in a mouse model of Alzheimer's disease. BMC neuroscience. https://doi.org/10.1186/s12868-022-00699-8
Vancouver
Cucos CA, Dobre M, Dragnea EM, Manda G, Milanesi E. Increased MYD88 blood transcript in a mouse model of Alzheimer's disease. BMC neuroscience. 2022. doi:10.1186/s12868-022-00699-8. PMID: 35277123.
BibTeX
@article{cucos2022-35277123,
author = {Cucos, C. A. and Dobre, M. and Dragnea, E. M. and Manda, G. and Milanesi, E.},
title = {{Increased MYD88 blood transcript in a mouse model of Alzheimer's disease}},
journal = {BMC neuroscience},
year = {2022},
doi = {10.1186/s12868-022-00699-8},
pmid = {35277123},
url = {https://doi.org/10.1186/s12868-022-00699-8}
}
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Key findings
- It has been shown that TLR/MYD88 signaling is involved in the chronic low-grade sterile inflammation associated with AD.
- Results Increased MYD88 transcript in the whole blood from AT mice as compared to WT controls was found, which seems to increase in time due to disease progression and not to aging.
- This finding suggests that blood leukocytes are primed to develop TLR/MYD-mediated inflammatory processes.
- Moreover, results indicate that MYD88 blood levels were not modulated by the diseases-specific treatment with Rivastigmine.
- Conclusions Our results suggest that MYD88 might be a promising blood biomarker to monitor AD progression.
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Study details
- Evidence strengthLow
How this study scored 43/100
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 25 of the 58 points we could judge it on, which is 43 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (BMC neuroscience) |
| 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 | 3 / 5 | 2022 — within 6 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 35277123) |
| Free to read | 2 / 2 | Free to read |
| Points | 25 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 25 of the 58 points we could judge it on is 43 out of 100. |
| Total | 43 / 100 | — |
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