Evidence map›Paper›PMID 38612701›Full record

ReviewInternational journal of molecular sciences2024

Alzheimer's Amyloid Hypothesis and Antibody Therapy: Melting Glaciers?

Poul F Høilund-Carlsen, Abass Alavi, Rudolph J Castellani, Rachael L Neve, George Perry, Mona-Elisabeth Revheim, Jorge R Barrio

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
12.1field-weighted citation impact, top 1% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Review
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  5. Article
  6. Review
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  13. In 2024, theFrontiers in aging neuroscience · 2024
    Article
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

7 authors at 7 institutions in 3 countries.

Poul F Høilund-CarlsenDepartment of Nuclear Medicine, Odense University Hospital, 5000 Odense C, Denmark.ORCID 0000-0001-7420-2367
Abass AlaviDepartment of Radiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.ORCID 0000-0002-2442-7901
Rudolph J CastellaniDepartment of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.ORCID 0000-0002-5414-3184
Rachael L NeveGene Delivery Technology Core, Massachusetts General Hospital, Boston, MA 02114, USA.ORCID 0000-0002-3854-5968
George PerryDepartment of Neuroscience, Developmental and Regenerative Biology and Genetics of Neurodegeneration, University of Texas at San Antonio, San Antonio, TX 78249, USA.ORCID 0000-0002-6547-0172
Mona-Elisabeth RevheimThe Intervention Centre, Division of Technology and Innovation, Oslo University Hospital, 0372 Oslo, Norway.ORCID 0000-0003-3300-7420
Jorge R BarrioDepartment of Molecular and Medical Pharmacology, David Geffen UCLA School of Medicine, Los Angeles, LA 90095, USA.ORCID 0000-0002-3743-9936
Massachusetts General Hospital · USNorthwestern University · USOslo University Hospital · NOThe University of Texas at San Antonio · USUniversity of California, Los Angeles · USUniversity of Pennsylvania · USUniversity of Southern Denmark · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The amyloid cascade hypothesis for Alzheimer's disease is still alive, although heavily challenged. Effective anti-amyloid immunotherapy would confirm the hypothesis' claim that the protein amyloid-beta is the cause of the disease. Two antibodies, aducanumab and lecanemab, have been approved by the U.S. Food and Drug Administration, while a third, donanemab, is under review. The main argument for the FDA approvals is a presumed therapy-induced removal of cerebral amyloid deposits. Lecanemab and donanemab are also thought to cause some statistical delay in the determination of cognitive decline. However, clinical efficacy that is less than with conventional treatment, selection of amyloid-positive trial patients with non-specific amyloid-PET imaging, and uncertain therapy-induced removal of cerebral amyloids in clinical trials cast doubt on this anti-Alzheimer's antibody therapy and hence on the amyloid hypothesis, calling for a more thorough investigation of the negative impact of this type of therapy on the brain.

Indexed as

Alzheimer DiseaseAntibodies, Monoclonal, HumanizedAmyloidogenic ProteinsHumansIce CoverRadioimmunotherapyUnited StatesAmyloidogenic ProteinsAntibodies, Monoclonal, HumanizeddonanemabAlzheimer’s diseaseamyloid-PETARIAATNCDR-SBMICDMMSERCT

Identifiers

PMID38612701
PMCPMC11012162
OpenAlexW4393356567

What Socratic 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 Socratic graph.