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CSF amyloid β38 as a novel diagnostic marker for dementia with Lewy bodies
Mulugeta E, Londos E, Ballard C, Alves G, Zetterberg H, Blennow K, Skogseth R, Minthon L et al.. Journal of neurology, neurosurgery, and psychiatry, 2010-11-03
Topic: Amyloid, tau and blood-test diagnosis
Plain-language summary
Background The clinical distinction between Alzheimer's disease (AD) and dementia with Lewy bodies (DLB) is sometimes difficult, particularly in mild cases. Although CSF markers such as amyloid β42 (Aβ42) and P-tau can distinguish between AD and normal controls, their ability to distinguish between AD and DLB is not adequate. Objective This study aims to investigate whether CSF markers, in particular levels of Aβ38, can differentiate between mild AD and DLB. Methods 85 individuals were included after standardised diagnostic procedures: 30 diagnosed as probable AD, 23 probable DLB, 20 probable Parkinson's disease dementia and 12 non-demented control subjects. CSF levels of Aβ38, Aβ40 and Aβ42 were determined using commercially available ultra-sensitive multi-array kit assay (MSD) for human Aβ peptides. Total tau (T-tau) and phosphorylated tau (P-tau) were analysed using ELISA (Innotest). In addition, combinations (Aβ42/Aβ38, Aβ42/Aβ40, Aβ42/P-tau and Aβ42/Aβ38/P-tau) were assessed. Results Significant between group differences were found for all CSF measures, and all except Aβ40, Aβ42 and Aβ42/P-tau differed between AD and DLB. The Aβ42/Aβ38 ratio was the measure that best discriminated between AD and DLB (AUC 0.765; p<0.005), with a sensitivity of 78% and a specificity of 67%. Conclusion This study suggests that the level of Aβ38 can potentially contribute in the diagnostic distinction between AD and DLB when combined with Aβ42. Single measures had low diagnostic accuracy, suggesting that developing a panel of markers is the most promising strategy. Studies with independent and larger samples and a priori cut-offs are needed to test this hypothesis.
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APA 7th
Mulugeta, E., Londos, E., Ballard, C., Alves, G., Zetterberg, H., Blennow, K., et al. (2011). CSF amyloid β38 as a novel diagnostic marker for dementia with Lewy bodies. Journal of neurology, neurosurgery, and psychiatry. https://doi.org/10.1136/jnnp.2009.199398
Vancouver
Mulugeta E, Londos E, Ballard C, Alves G, Zetterberg H, Blennow K, et al. CSF amyloid β38 as a novel diagnostic marker for dementia with Lewy bodies. Journal of neurology, neurosurgery, and psychiatry. 2011. doi:10.1136/jnnp.2009.199398. PMID: 21047883.
BibTeX
@article{mulugeta2011-21047883,
author = {Mulugeta, E. and Londos, E. and Ballard, C. and Alves, G. and Zetterberg, H. and Blennow, K. and Skogseth, R. and Minthon, L. and others},
title = {{CSF amyloid β38 as a novel diagnostic marker for dementia with Lewy bodies}},
journal = {Journal of neurology, neurosurgery, and psychiatry},
year = {2011},
doi = {10.1136/jnnp.2009.199398},
pmid = {21047883},
url = {https://doi.org/10.1136/jnnp.2009.199398}
}
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Key findings
- Results Significant between group differences were found for all CSF measures, and all except Aβ40, Aβ42 and Aβ42/P-tau differed between AD and DLB.
- Conclusion This study suggests that the level of Aβ38 can potentially contribute in the diagnostic distinction between AD and DLB when combined with Aβ42.
- Single measures had low diagnostic accuracy, suggesting that developing a panel of markers is the most promising strategy.
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Study details
- Participants85
- Effect sizeAUC 0.765
- Evidence strengthLow
How this study scored 48/100
Published in a peer-reviewed journal. Scored zero for study design and randomized / 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 multicenter 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 (Journal of neurology, neurosurgery, and psychiatry) |
| 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 | 1 / 4 | 85 participants |
| Effect reported | 3 / 3 | Effect reported with a statistic (interval, p-value, ratio or similar) |
| Studied in people | 3 / 3 | Studied in people (participant count stated) |
| Randomized / blinded | 0 / 2 | No randomization 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 |
| Multicenter collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 21047883) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| 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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