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[Anti-Amyloid Antibody Therapy for Alzheimer's Disease]
Moeko Shinohara, Kenjiro Ono. Brain and nerve = Shinkei kenkyu no shinpo, 2024-10
Topic: Disease mechanisms in lab and animal studies
Plain-language summary
Alzheimer's disease (AD) is pathologically characterized by deposition of amyloid plaques (comprising amyloid β [Aβ] protein) and neurofibrillary tangles (comprising tau protein), and neuronal death. Aβ monomers aggregate to form oligomers, protofibrils, and mature fibrils. Previously, the mature fibrils and plaques were implicated as contributors to neurotoxicity and neurodegeneration. However, a growing body of evidence proves stronger toxicity of oligomers and protofibrils. Among the many recent phase 3 clinical trials that have investigated the role of anti-Aβ antibodies in AD, some have shown the clinical efficacy of aducanumab, lecanemab, and donanemab in these patients. Lecanemab showed selectivity towards protofibrils over fibrils, and donanemab was specifically directed against Aβ only in brain-specific amyloid plaques. In contrast, other anti-Aβ antibodies did not show efficacy in AD.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Shinohara, M., & Ono, K. (2024). [Anti-Amyloid Antibody Therapy for Alzheimer's Disease]. Brain and nerve = Shinkei kenkyu no shinpo. https://doi.org/10.11477/mf.1416202747
Vancouver
Shinohara M, Ono K. [Anti-Amyloid Antibody Therapy for Alzheimer's Disease]. Brain and nerve = Shinkei kenkyu no shinpo. 2024. doi:10.11477/mf.1416202747. PMID: 39370836.
BibTeX
@article{shinohara2024-39370836,
author = {Shinohara, Moeko and Ono, Kenjiro},
title = {{[Anti-Amyloid Antibody Therapy for Alzheimer's Disease]}},
journal = {Brain and nerve = Shinkei kenkyu no shinpo},
year = {2024},
doi = {10.11477/mf.1416202747},
pmid = {39370836},
url = {https://doi.org/10.11477/mf.1416202747}
}
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Key findings
- Previously, the mature fibrils and plaques were implicated as contributors to neurotoxicity and neurodegeneration.
- However, a growing body of evidence proves stronger toxicity of oligomers and protofibrils.
- Among the many recent phase 3 clinical trials that have investigated the role of anti-Aβ antibodies in AD, some have shown the clinical efficacy of aducanumab, lecanemab, and donanemab in these patients.
- Lecanemab showed selectivity towards protofibrils over fibrils, and donanemab was specifically directed against Aβ only in brain-specific amyloid plaques.
- In contrast, other anti-Aβ antibodies did not show efficacy in AD.
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Study details
- Study designclinical trial
- Evidence strengthLow
How this study scored 43/100
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 24 of the 56 points we could judge it on, which is 43 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Brain and nerve = Shinkei kenkyu no shinpo) |
| 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 | 4 / 5 | 2024 — within 3 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 39370836) |
| Free to read | — / 2 | Access not recorded — left out of this score |
| Points | 24 / 56 | Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 24 of the 56 points we could judge it on is 43 out of 100. |
| Total | 43 / 100 | — |
What each of these 20 components measures, and what this score is not →
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