Evidence map›Paper›PMID 33575481›Full record

ReviewNeurology. Genetics2021

Can Anti-β-amyloid Monoclonal Antibodies Work in Autosomal Dominant Alzheimer Disease?

Bruno P Imbimbo, Ugo Lucca, Mark Watling

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Neurology. Genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
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  3. Article
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  5. Article
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  7. Article
  8. The evolutionary origins of dementia.Journal of Alzheimer's disease reports
    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

3 authors at 1 institution in 2 countries.

Bruno P ImbimboDepartment of Research & Development (B.P.I.), Chiesi Farmaceutici, Parma, Italy; Laboratory of Geriatric Neuropsychiatry (U.L.), Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milano, Italy; and CNS & Pain Department (M.W.), TranScrip Partners, Reading, United Kingdom.ORCID 0000-0002-0327-7262
Ugo LuccaDepartment of Research & Development (B.P.I.), Chiesi Farmaceutici, Parma, Italy; Laboratory of Geriatric Neuropsychiatry (U.L.), Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milano, Italy; and CNS & Pain Department (M.W.), TranScrip Partners, Reading, United Kingdom.
Mark WatlingDepartment of Research & Development (B.P.I.), Chiesi Farmaceutici, Parma, Italy; Laboratory of Geriatric Neuropsychiatry (U.L.), Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milano, Italy; and CNS & Pain Department (M.W.), TranScrip Partners, Reading, United Kingdom.
Mario Negri Institute for Pharmacological Research · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The dominant theory of Alzheimer disease (AD) has been that amyloid-β (Aβ) accumulation in the brain is the initial cause of the degeneration leading to cognitive and functional deficits. Autosomal dominant Alzheimer disease (ADAD), in which pathologic mutations of the amyloid precursor protein (

Identifiers

PMID33575481
PMCPMC7862085
OpenAlexW3112207405

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.