Evidence map›Paper›PMID 39865265›Full record

ReviewTranslational neurodegeneration2025

Second-generation anti-amyloid monoclonal antibodies for Alzheimer's disease: current landscape and future perspectives.

Byeong-Hyeon Kim, Sujin Kim, Yunkwon Nam, Yong Ho Park, Seong Min Shin, Minho Moon

Abstract readReview
In one paragraph

Review in Translational neurodegeneration, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 4 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

85 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Reply to "Pooling Alzheimer's disease: when methodological rigor risks obscuring biological complexity".Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

25 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Byeong-Hyeon Kim *Department of Biochemistry, College of Medicine, Konyang University, 158, Gwanjeodong-Ro Seo-Gu, Daejeon, 35365, Republic of Korea.
Sujin Kim *Department of Biochemistry, College of Medicine, Konyang University, 158, Gwanjeodong-Ro Seo-Gu, Daejeon, 35365, Republic of Korea.
Yunkwon Nam *Department of Biochemistry, College of Medicine, Konyang University, 158, Gwanjeodong-Ro Seo-Gu, Daejeon, 35365, Republic of Korea.
Yong Ho Park *Department of Biochemistry, College of Medicine, Konyang University, 158, Gwanjeodong-Ro Seo-Gu, Daejeon, 35365, Republic of Korea.
Seong Min Shin *Department of Biochemistry, College of Medicine, Konyang University, 158, Gwanjeodong-Ro Seo-Gu, Daejeon, 35365, Republic of Korea.
Minho MoonDepartment of Biochemistry, College of Medicine, Konyang University, 158, Gwanjeodong-Ro Seo-Gu, Daejeon, 35365, Republic of Korea. hominmoon@konyang.ac.kr.ORCID http://orcid.org/0000-0002-8140-5928

Funding

Korea Health Industry Development Institute RS-2023-KH138733National Research Foundation of Korea NRF-2022R1A6A3A13053190National Research Foundation of Korea RS-2023-00212388National Research Foundation of Korea RS-2023-00240010National Research Foundation of Korea RS-2023-00273557National Research Foundation of Korea RS-2024-00450135
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common type of dementia. Monoclonal antibodies (MABs) serve as a promising therapeutic approach for AD by selectively targeting key pathogenic factors, such as amyloid-β (Aβ) peptide, tau protein, and neuroinflammation. Specifically, based on their efficacy in removing Aβ plaques from the brains of patients with AD, the U.S. Food and Drug Administration has approved three anti-amyloid MABs, aducanumab (Aduhelm®), lecanemab (Leqembi®), and donanemab (Kisunla™). Notably, lecanemab received traditional approval after demonstrating clinical benefit, supporting the Aβ cascade hypothesis. These MABs targeting Aβ are categorized based on their affinity to diverse conformational features of Aβ, including monomer, fibril, protofibril, and plaque forms of Aβ as well as pyroglutamate Aβ. First-generation MABs targeting the non-toxic monomeric Aβ, such as solanezumab, bapineuzumab, and crenezumab, failed to demonstrate clinical benefit for AD in clinical trials. In contrast, second-generation MABs, including aducanumab, lecanemab, donanemab, and gantenerumab directed against pathogenic Aβ species and aggregates have shown that reducing Aβ deposition can be an effective strategy to slow cognitive impairment in AD. In this review, we provide a comprehensive overview of the current status, mechanisms, outcomes, and limitations of second-generation MABs for the clinical treatment of AD. Moreover, we discuss the perspectives and future directions of anti-amyloid MABs in the treatment of AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAntibodies, MonoclonalAnimalsAntibodies, Monoclonal, HumanizedHumansPlaque, AmyloidaducanumabAmyloid beta-PeptidesAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAducanumabAlzheimer’s diseaseAmyloid-related imaging abnormalitiesDonanemabGantenerumabLecanemab

Identifiers

PMID39865265
PMCPMC11771116

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.