Evidence map›Paper›PMID 38001337›Full record

ReviewMolecular psychiatry2024

Clarity on the blazing trail: clearing the way for amyloid-removing therapies for Alzheimer's disease.

Yan Lian, Yu-Juan Jia, Joelyn Wong, Xin-Fu Zhou, Weihong Song, Junhong Guo, Colin L Masters, Yan-Jiang Wang

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular psychiatry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.0field-weighted citation impact, top 8% of its field
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

14 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
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  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
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  13. Do anti-Aβ monoclonal antibodies lower brain plaques in Alzheimer patients through microglia activation?Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  14. Review
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

8 authors at 5 institutions in 2 countries.

Yan Lian *Department of Prevention and Health Care, Daping Hospital, Third Military Medical University, Chongqing, China.
Yu-Juan Jia *Department of Neurology, First Hospital of Shanxi Medical University, Taiyuan, China.
Joelyn WongThe Florey Institute, The University of Melbourne, Parkville, VIC, Australia.
Xin-Fu ZhouSchool of Pharmacy and Medical Sciences and Sansom Institute, Division of Health Sciences, University of South Australia, Adelaide, SA, Australia.
Weihong SongInstitute of Aging, Key Laboratory of Alzheimer's Disease of Zhejiang Province. Zhejiang Clinical Research Center for Mental Disorders, School of Mental Health and The Affiliated Kangning Hospital, Wenzhou Medical University, Oujiang Laboratory (Zhejiang Laboratory for Regenerative Medicine, Vision and Brain Health), Wenzhou, Zhejiang, China.ORCID 0000-0001-9928-889X
Junhong GuoDepartment of Neurology, First Hospital of Shanxi Medical University, Taiyuan, China. neuroguo@163.com.
Colin L MastersThe Florey Institute, The University of Melbourne, Parkville, VIC, Australia. c.masters@unimelb.edu.au.
Yan-Jiang WangDepartment of Neurology and Centre for Clinical Neuroscience, Daping Hospital, Third Military Medical University, Chongqing, China. yanjiang_wang@tmmu.edu.cn.ORCID 0000-0002-6227-6112
Army Medical University · CNShanxi Medical University · CNThe University of Melbourne · AUUniversity of South Australia · AUWenzhou Medical University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81930028National Natural Science Foundation of China (National Science Foundation of China) 82120108010
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder with a complex pathogenesis. Senile plaques composed of the amyloid-β (Aβ) peptide in the brain are the core hallmarks of AD and a promising target for the development of disease-modifying therapies. However, over the past 20 years, the failures of clinical trials directed at Aβ clearance have fueled a debate as to whether Aβ is the principal pathogenic factor in AD and a valid therapeutic target. The success of the recent phase 3 trials of lecanemab (Clarity AD) and donanemab (Trailblazer Alz2), and lessons from previous Aβ clearance trials provide critical evidence to support the role of Aβ in AD pathogenesis and suggest that targeting Aβ clearance is heading in the right direction for AD treatment. Here, we analyze key questions relating to the efficacy of Aβ targeting therapies, and provide perspectives on early intervention, adequate Aβ removal, sufficient treatment period, and combinatory therapeutics, which may be required to achieve the best cognitive benefits in future trials in the real world.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesBrainPlaque, AmyloidAmyloidAntibodies, Monoclonal, HumanizedHumansAmyloidAmyloid beta-PeptidesAntibodies, Monoclonal, Humanized

Identifiers

PMID38001337
OpenAlexW4388974828

What OpenQuestion holds

Textmetadata
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.