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Elevated soluble amyloid beta protofibrils in Down syndrome and Alzheimer's disease
Malin Johannesson, Charlotte Sahlin, Linda Söderberg, Hans Basun, Johanna Fälting, Christer Möller, Olof Zachrisson, Dan Sunnemark et al.. Molecular and cellular neurosciences, 2021-06-04
Topic: Plasma and spinal-fluid biomarkers
Down syndrome (DS) is caused by trisomy of chromosome 21, which leads to a propensity to develop amyloid β (Aβ) brain pathology in early adulthood followed later by cognitive and behavioral deterioration. Characterization of the Aβ pathology is important to better understand the clinical deterioration of DS individuals and to identify interventive strategies. Brain samples from people with DS and Alzheimer's disease (AD), as well as non-demented controls (NDC), were analyzed with respect to different Aβ species. Immunohistochemical staining using antibodies towards Aβ was also performed. Elevated levels of soluble Aβ protofibrils and insoluble Aβx-40 and Aβx-42 in formic acid brain extracts, and elevated immunohistochemical staining of Aβ deposits were demonstrated with the antibody BAN2401 (lecanemab) in DS and AD compared with NDC. These data and the promising data in a large phase 2 CE clinical trial with lecanemab suggest that lecanemab may have the potential to preserve cognitive capacity in DS. Lecanemab is currently in a phase 3 CE clinical trial.
Key findings
- Elevated levels of soluble Aβ protofibrils and insoluble Aβx-40 and Aβx-42 in formic acid brain extracts, and elevated immunohistochemical staining of Aβ deposits were demonstrated with the antibody BAN2401 (lecanemab) in DS and AD compared with NDC.
- These data and the promising data in a large phase 2 CE clinical trial with lecanemab suggest that lecanemab may have the potential to preserve cognitive capacity in DS.
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Study details
- Study designclinical trial
- Evidence strengthLow
How this study scored 41/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people 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, multi-centre collaboration and free to read, so those were left out: it earned 23 of the 56 points we could judge it on, which is 41 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Molecular and cellular neurosciences) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 0 / 12 | Design recorded as “clinical trial”, which our rubric does not rank (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 | 2021 — 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 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| 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 34091073) |
| Free to read | — / 2 | Access not recorded — left out of this score |
| Points | 23 / 56 | Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 23 of the 56 points we could judge it on is 41 out of 100. |
| Total | 41 / 100 | — |
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APA 7th
Johannesson, M., Sahlin, C., Söderberg, L., Basun, H., Fälting, J., Möller, C., et al. (2021). Elevated soluble amyloid beta protofibrils in Down syndrome and Alzheimer's disease. Molecular and cellular neurosciences. https://doi.org/10.1016/j.mcn.2021.103641
Vancouver
Johannesson M, Sahlin C, Söderberg L, Basun H, Fälting J, Möller C, et al. Elevated soluble amyloid beta protofibrils in Down syndrome and Alzheimer's disease. Molecular and cellular neurosciences. 2021. doi:10.1016/j.mcn.2021.103641. PMID: 34091073.
BibTeX
@article{johannesson2021-34091073,
author = {Johannesson, Malin and Sahlin, Charlotte and Söderberg, Linda and Basun, Hans and Fälting, Johanna and Möller, Christer and Zachrisson, Olof and Sunnemark, Dan and others},
title = {{Elevated soluble amyloid beta protofibrils in Down syndrome and Alzheimer's disease}},
journal = {Molecular and cellular neurosciences},
year = {2021},
doi = {10.1016/j.mcn.2021.103641},
pmid = {34091073},
url = {https://doi.org/10.1016/j.mcn.2021.103641}
}