Evidence map›Paper›PMID 28327340›Full record

ReviewThe Lancet. Neurology2017

Epileptic activity in Alzheimer's disease: causes and clinical relevance.

Keith A Vossel, Maria C Tartaglia, Haakon B Nygaard, Adam Z Zeman, Bruce L Miller

Registry-linked trialAbstract readReview
In one paragraph

Review in The Lancet. Neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03617497 (Prevalence of Epilepsy and Sleep Wake Disorders in Alzheimer Disease), which is not on this map. Cited by 341 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
341citing papers in PubMed, 3 pooled it
23.3field-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.

NCT03617497 naunknown statusnot on this mapstarted 2020, after this paper: background citation

Prevalence of Epilepsy and Sleep Wake Disorders in Alzheimer Disease

TypeinterventionalSponsorUniversitaire Ziekenhuizen KU LeuvenRan2020 to 2024Enrolled78ConditionsAlzheimer Disease, Alzheimer Dementia, Epilepsy, Sleep Wake DisordersArmsscalp EEG and polysomnography, scalp EEG with foramen ovale electrodes with polysomnography
3 · Its place in the literature

Who cites it

341 citing papers in PubMed, 3 syntheses or guidelines pooled it, 587 citations in OpenAlex.

  1. Pooled it
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  10. The Alzheimer's disease risk gene SORL1 is a regulator of excitatory neuronal function.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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281 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 5 institutions in 3 countries.

Keith A VosselMemory and Aging Center, Department of Neurology, University of California, San Francisco, CA, USA. Electronic address: kvossel@umn.edu.
Maria C TartagliaDepartment of Neurology, University of Toronto, ON, Canada.
Haakon B NygaardDivision of Neurology, University of British Columbia, Vancouver, BC, Canada.
Adam Z ZemanCognitive Neurology Research Group, University of Exeter Medical School, Exeter, UK.
Bruce L MillerMemory and Aging Center, Department of Neurology, University of California, San Francisco, CA, USA.
University Memory and Aging Center · USUniversity of British Columbia · CAUniversity of California, San Francisco · USUniversity of Exeter · GBUniversity of Toronto · CA

Funding

TDP-43 Loss-of-Function: Biology to BiomarkersP01AG019724 · NIA · UNIVERSITY OF PENNSYLVANIA · PI Jennifer Merrilees · 2002 to 2026
$67.2M
PrPSc SPECIFIC INTERACTION WITH NOVEL PrP-Fc FUSION PROTEINSP50AG023501 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MILLER, BRUCE L · 2004 to 2018
$27.1M
Mechanisms and Treatment of Network Dysfunction in Alzheimer's DiseaseK23AG038357 · NIA · J. DAVID GLADSTONE INSTITUTES · PI VOSSEL, KEITH ALAN · 2011 to 2015
$764k
NIA NIH HHS K23 AG038357NIA NIH HHS P01 AG019724NIA NIH HHS P50 AG023501
6 · The paper itself

Abstract

Epileptic activity is frequently associated with Alzheimer's disease; this association has therapeutic implications, because epileptic activity can occur at early disease stages and might contribute to pathogenesis. In clinical practice, seizures in patients with Alzheimer's disease can easily go unrecognised because they usually present as non-motor seizures, and can overlap with other symptoms of the disease. In patients with Alzheimer's disease, seizures can hasten cognitive decline, highlighting the clinical relevance of early recognition and treatment. Some evidence indicates that subclinical epileptiform activity in patients with Alzheimer's disease, detected by extended neurophysiological monitoring, can also lead to accelerated cognitive decline. Treatment of clinical seizures in patients with Alzheimer's disease with select antiepileptic drugs (AEDs), in low doses, is usually well tolerated and efficacious. Moreover, studies in mouse models of Alzheimer's disease suggest that certain classes of AEDs that reduce network hyperexcitability have disease-modifying properties. These AEDs target mechanisms of epileptogenesis involving amyloid β and tau. Clinical trials targeting network hyperexcitability in patients with Alzheimer's disease will identify whether AEDs or related strategies could improve their cognitive symptoms or slow decline.

Indexed as

Alzheimer DiseaseAnimalsAnticonvulsantsEpilepsyHumansAnticonvulsants

Identifiers

PMID28327340
PMCPMC5973551
OpenAlexW2599512437

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.