Evidence map›Paper›PMID 34117482›Full record

ReviewNature reviews. Neurology2021

Amyloid-β: a potential link between epilepsy and cognitive decline.

Michele Romoli, Arjune Sen, Lucilla Parnetti, Paolo Calabresi, Cinzia Costa

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 4 pooled it
16.6field-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

78 citing papers in PubMed, 4 syntheses or guidelines pooled it, 130 citations in OpenAlex.

  1. Pooled it
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  8. Risk of epilepsy in people with adult-onset hydrocephalus: insights from the UK Biobank.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
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  18. Burden of psychiatric disease inversely correlates with Alzheimer's age at onset.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
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18 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

5 authors at 3 institutions in 2 countries.

Michele RomoliNeurology Clinic, Department of Medicine and Surgery, University of Perugia - S. Maria della Misericordia Hospital, Perugia, Italy.ORCID http://orcid.org/0000-0001-8009-8543
Arjune SenOxford Epilepsy Research Group, NIHR Biomedical Research Centre, Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, Oxford, UK.ORCID http://orcid.org/0000-0002-8948-4763
Lucilla ParnettiNeurology Clinic, Department of Medicine and Surgery, University of Perugia - S. Maria della Misericordia Hospital, Perugia, Italy.
Paolo CalabresiDipartimento di Neuroscienze, Università Cattolica del Sacro Cuore, Rome, Italy.
Cinzia CostaNeurology Clinic, Department of Medicine and Surgery, University of Perugia - S. Maria della Misericordia Hospital, Perugia, Italy. cinzia.costa@unipg.it.ORCID http://orcid.org/0000-0002-4862-4221
University of Perugia · ITJohn Radcliffe Hospital · GBUniversità Cattolica del Sacro Cuore · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

People with epilepsy - in particular, late-onset epilepsy of unknown aetiology - have an elevated risk of dementia, and seizures have been detected in the early stages of Alzheimer disease (AD), supporting the concept of an epileptic AD prodrome. However, the relationship between epilepsy and cognitive decline remains controversial, with substantial uncertainties about whether epilepsy drives cognitive decline or vice versa, and whether shared pathways underlie both conditions. Here, we review evidence that amyloid-β (Aβ) forms part of a shared pathway between epilepsy and cognitive decline, particularly in the context of AD. People with epilepsy show an increased burden of Aβ pathology in the brain, and Aβ-mediated epileptogenic alterations have been demonstrated in experimental studies, with evidence suggesting that Aβ pathology might already be pro-epileptogenic at the soluble stage, long before plaque deposition. We discuss the hypothesis that Aβ mediates - or is at least a major determinant of - a continuum spanning epilepsy and cognitive decline. Serial cognitive testing and assessment of Aβ levels might be worthwhile to stratify the risk of developing dementia in people with late-onset epilepsy. If seizures are a clinical harbinger of dementia, people with late-onset epilepsy could be an ideal group in which to implement preventive or therapeutic strategies to slow cognitive decline.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainClinical Trials as TopicCognitive DysfunctionEpilepsyHumansMental Status and Dementia TestsObservational Studies as TopicPlaque, AmyloidRisk FactorsAmyloid beta-Peptides

Identifiers

PMID34117482
OpenAlexW3167249883

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.