Evidence map›Paper›PMID 30610216›Full record

ReviewNature reviews. Neurology2019

A critical appraisal of amyloid-β-targeting therapies for Alzheimer disease.

Francesco Panza, Madia Lozupone, Giancarlo Logroscino, Bruno P Imbimbo

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Neurology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 425 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
425citing papers in PubMed, 6 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

425 citing papers in PubMed, 6 syntheses or guidelines pooled it.

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  3. Efficacy of anti-amyloid-ß monoclonal antibody therapy in early Alzheimer's disease: a systematic review and meta-analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024
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  17. International journal of molecular sciences · 2026
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365 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

4 authors.

Francesco Panza *Neurodegenerative Disease Unit, Department of Basic Medicine, Neuroscience and Sense Organs, University of Bari Aldo Moro, Bari, Italy. geriat.dot@uniba.it.ORCID http://orcid.org/0000-0002-7220-0656
Madia LozuponeNeurodegenerative Disease Unit, Department of Basic Medicine, Neuroscience and Sense Organs, University of Bari Aldo Moro, Bari, Italy.
Giancarlo LogroscinoNeurodegenerative Disease Unit, Department of Basic Medicine, Neuroscience and Sense Organs, University of Bari Aldo Moro, Bari, Italy.
Bruno P Imbimbo *Department of Research and Development, Chiesi Farmaceutici, Parma, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Brain accumulation of the amyloid-β (Aβ) peptide is believed to be the initial event in the Alzheimer disease (AD) process. Aβ accumulation begins 15-20 years before clinical symptoms occur, mainly owing to defective brain clearance of the peptide. Over the past 20 years, we have seen intensive efforts to decrease the levels of Aβ monomers, oligomers, aggregates and plaques using compounds that decrease production, antagonize aggregation or increase brain clearance of Aβ. Unfortunately, these approaches have failed to show clinical benefit in large clinical trials involving patients with mild to moderate AD. Clinical trials in patients at earlier stages of the disease are ongoing, but the initial results have not been clinically impressive. Efforts are now being directed against Aβ oligomers, the most neurotoxic molecular species, and monoclonal antibodies directed against these oligomers are producing encouraging results. However, Aβ oligomers are in equilibrium with both monomeric and aggregated species; thus, previous drugs that efficiently removed monomeric Aβ or Aβ plaques should have produced clinical benefits. In patients with sporadic AD, Aβ accumulation could be a reactive compensatory response to neuronal damage of unknown cause, and alternative strategies, including interference with modifiable risk factors, might be needed to defeat this devastating disease.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid Precursor Protein SecretasesAnimalsAntibodies, Monoclonal, HumanizedAspartic Acid EndopeptidasesDrug Delivery SystemsHumansaducanumabAmyloid beta-PeptidesAmyloid Precursor Protein SecretasesAntibodies, Monoclonal, HumanizedAspartic Acid EndopeptidasesBACE1 protein, human

Identifiers

PMID30610216

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.