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Different pattern of CSF glial markers between dementia with Lewy bodies and Alzheimer's disease
Morenas-Rodríguez E, Alcolea D, Suárez-Calvet M, Muñoz-Llahuna L, Vilaplana E, Sala I, Subirana A, Querol-Vilaseca M et al.. Scientific reports, 2019-05-24
Topic: Amyloid, tau and blood-test diagnosis
The role of innate immunity in dementia with Lewy bodies (DLB) has been little studied. We investigated the levels in cerebrospinal fluid (CSF) of glial proteins YKL-40, soluble TREM2 (sTREM2) and progranulin in DLB and their relationship with Alzheimer's disease (AD) biomarkers. We included patients with DLB (n = 37), prodromal DLB (prodDLB, n = 23), AD dementia (n = 50), prodromal AD (prodAD, n = 53), and cognitively normal subjects (CN, n = 44). We measured levels of YKL-40, sTREM2, progranulin, Aβ 1-42 , total tau (t-tau) and phosphorylated tau (p-tau) in CSF. We stratified the group DLB according to the ratio t-tau/Aβ 1-42 (≥0.52, indicative of AD pathology) and the A/T classification. YKL-40, sTREM2 and progranulin levels did not differ between DLB groups and CN. YKL-40 levels were higher in AD and prodAD compared to CN and to DLB and prodDLB. Patients with DLB with a CSF profile suggestive of AD copathology had higher levels of YKL-40, but not sTREM2 or PGRN, than those without. T+ DLB patients had also higher YKL-40 levels than T-. Of these glial markers, only YKL-40 correlated with t-tau and p-tau in DLB and in prodDLB. In contrast, in prodAD, sTREM2 and PGRN also correlated with t-tau and p-tau. In conclusion, sTREM2 and PGRN are not increased in the CSF of DLB patients. YKL-40 is only increased in DLB patients with an AD biomarker profile, suggesting that the increase is driven by AD-related neurodegeneration. These data suggest a differential glial activation between DLB and AD.
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APA 7th
Morenas-Rodríguez, E., Alcolea, D., Suárez-Calvet, M., Muñoz-Llahuna, L., Vilaplana, E., Sala, I., et al. (2019). Different pattern of CSF glial markers between dementia with Lewy bodies and Alzheimer's disease. Scientific reports. https://doi.org/10.1038/s41598-019-44173-8
Vancouver
Morenas-Rodríguez E, Alcolea D, Suárez-Calvet M, Muñoz-Llahuna L, Vilaplana E, Sala I, et al. Different pattern of CSF glial markers between dementia with Lewy bodies and Alzheimer's disease. Scientific reports. 2019. doi:10.1038/s41598-019-44173-8. PMID: 31127154.
BibTeX
@article{morenasrodriguez2019-31127154,
author = {Morenas-Rodríguez, E. and Alcolea, D. and Suárez-Calvet, M. and Muñoz-Llahuna, L. and Vilaplana, E. and Sala, I. and Subirana, A. and Querol-Vilaseca, M. and others},
title = {{Different pattern of CSF glial markers between dementia with Lewy bodies and Alzheimer's disease}},
journal = {Scientific reports},
year = {2019},
doi = {10.1038/s41598-019-44173-8},
pmid = {31127154},
url = {https://doi.org/10.1038/s41598-019-44173-8}
}
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Key findings
- YKL-40 levels were higher in AD and prodAD compared to CN and to DLB and prodDLB.
- In conclusion, sTREM2 and PGRN are not increased in the CSF of DLB patients.
- YKL-40 is only increased in DLB patients with an AD biomarker profile, suggesting that the increase is driven by AD-related neurodegeneration.
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Study details
- Participants37
- Evidence strengthLow
How this study scored 48/100
Published in a peer-reviewed journal. Scored zero for study design, 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 28 of the 58 points we could judge it on, which is 48 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Scientific reports) |
| 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 | 2 / 5 | 2019 — within 10 year(s) of the newest study here |
| Sample size | 1 / 4 | 37 participants |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 3 / 3 | Studied in people (participant count stated) |
| 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 31127154) |
| Free to read | 2 / 2 | Free to read |
| Points | 28 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 28 of the 58 points we could judge it on is 48 out of 100. |
| Total | 48 / 100 | — |
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