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Amyloid pathology influences aβ1-42 cerebrospinal fluid levels in dementia with lewy bodies
Sylvie Slaets, Nathalie Le Bastard, Jessie Theuns, Kristel Sleegers, Aline Verstraeten, Evelyn De Leenheir, Jill Luyckx, Jean-Jacques Martin et al.. Journal of Alzheimer's disease : JAD, 2013
Topic: Plasma and spinal-fluid biomarkers
A significant proportion of patients with dementia with Lewy bodies (DLB) show Alzheimer's disease (AD) pathology like senile plaques and neurofibrillary tangles. Biomarkers in cerebrospinal fluid (CSF), such as amyloid-β1-42 (Aβ1-42), total tau (T-tau), and hyperphosphorylated tau (P-tau181P), are linked to the different pathological hallmarks of AD. We set up a study to investigate the influence of AD co-pathology on CSF biomarker concentrations and profiles in autopsy-confirmed DLB. DLB patients with senile plaques showed significantly lower CSF Aβ1-42 concentrations than DLB patients without senile plaques, but not compared to the AD patients. There were no significant differences in CSF T-tau or P-tau181P concentrations between DLB patients with and without neurofibrillary tangles. A correlation was found between the number of APOE ε4 alleles and Aβ1-42 CSF levels in DLB patients with senile plaques. Although the CSF biomarkers Aβ1-42, T-tau, and P-tau181P have an added diagnostic value for the differential dementia diagnosis, concomitant amyloid pathology in DLB limits the use of CSF Aβ1-42 for the differential diagnosis of AD versus DLB.
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APA 7th
Slaets, S., Le Bastard, N., Theuns, J., Sleegers, K., Verstraeten, A., De Leenheir, E., et al. (2013). Amyloid pathology influences aβ1-42 cerebrospinal fluid levels in dementia with lewy bodies. Journal of Alzheimer's disease : JAD. https://doi.org/10.3233/jad-122176
Vancouver
Slaets S, Le Bastard N, Theuns J, Sleegers K, Verstraeten A, De Leenheir E, et al. Amyloid pathology influences aβ1-42 cerebrospinal fluid levels in dementia with lewy bodies. Journal of Alzheimer's disease : JAD. 2013. doi:10.3233/jad-122176. PMID: 23364139.
BibTeX
@article{slaets2013-23364139,
author = {Slaets, Sylvie and Le Bastard, Nathalie and Theuns, Jessie and Sleegers, Kristel and Verstraeten, Aline and De Leenheir, Evelyn and Luyckx, Jill and Martin, Jean-Jacques and others},
title = {{Amyloid pathology influences aβ1-42 cerebrospinal fluid levels in dementia with lewy bodies}},
journal = {Journal of Alzheimer's disease : JAD},
year = {2013},
doi = {10.3233/jad-122176},
pmid = {23364139},
url = {https://doi.org/10.3233/jad-122176}
}
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Key findings
- A significant proportion of patients with dementia with Lewy bodies (DLB) show Alzheimer's disease (AD) pathology like senile plaques and neurofibrillary tangles.
- DLB patients with senile plaques showed significantly lower CSF Aβ1-42 concentrations than DLB patients without senile plaques, but not compared to the AD patients.
- There were no significant differences in CSF T-tau or P-tau181P concentrations between DLB patients with and without neurofibrillary tangles.
- Although the CSF biomarkers Aβ1-42, T-tau, and P-tau181P have an added diagnostic value for the differential dementia diagnosis, concomitant amyloid pathology in DLB limits the use of CSF Aβ1-42 for the differential diagnosis of AD versus DLB.
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Study details
- Evidence strengthLow
How this study scored 38/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people 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, multicenter collaboration and free to read, so those were left out: it earned 21 of the 56 points we could judge it on, which is 38 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Journal of Alzheimer's disease : JAD) |
| 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 | 2013 — 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 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| 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 23364139) |
| Free to read | — / 2 | Access not recorded — left out of this score |
| Points | 21 / 56 | Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 21 of the 56 points we could judge it on is 38 out of 100. |
| Total | 38 / 100 | — |
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