Evidence map›Paper›PMID 42216470›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2026

Sleep-like slow waves during resting-state: A promising EEG biomarker of amyloid and neurodegeneration in preclinical Alzheimer's disease.

Pierre Champetier, Claudia Albero, Filipa Raposo Pereira, Rubén Herzog, Maximilien Chaumon, Marion Houot, Maxime Locatelli, Aurélie Kas, Marie-Odile Habert, Marc Teichmann and 5 more

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In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

15 authors.

Pierre ChampetierParis Brain Institute (ICM), Sorbonne University, Inserm, CNRS, Paris, France.ORCID https://orcid.org/0000-0003-0228-6084
Claudia AlberoParis Brain Institute (ICM), Sorbonne University, Inserm, CNRS, Paris, France.
Filipa Raposo PereiraParis Brain Institute (ICM), Sorbonne University, Inserm, CNRS, Paris, France.ORCID https://orcid.org/0000-0001-6199-7164
Rubén HerzogParis Brain Institute (ICM), Sorbonne University, Inserm, CNRS, Paris, France.ORCID https://orcid.org/0000-0002-3498-5819
Maximilien ChaumonParis Brain Institute (ICM), Sorbonne University, Inserm, CNRS, Paris, France.ORCID https://orcid.org/0000-0001-9664-8861
Marion HouotParis Brain Institute (ICM), Sorbonne University, Inserm, CNRS, Paris, France.ORCID https://orcid.org/0000-0002-3684-1763
Maxime LocatelliParis Brain Institute (ICM), Sorbonne University, Inserm, CNRS, Paris, France.ORCID https://orcid.org/0000-0003-2235-6457
Aurélie KasInserm, CNRS, laboratoire d'imagerie biomédicale, service de médecine nucléaire, groupe hospitalier Pitié-Salpêtrière, Sorbonne université, AP-HP, Paris, France.
Marie-Odile HabertCATI US52-UAR2031, CEA, ICM, Sorbonne Université, CNRS, INSERM, APHP, Paris, France.ORCID https://orcid.org/0000-0002-7719-9746
Marc TeichmannDépartement de Neurologie, Institut de la Mémoire et de la Maladie d'Alzheimer (IM2A), Paris, France.
Stéphane EpelbaumParis Brain Institute (ICM), Sorbonne University, Inserm, CNRS, Paris, France.ORCID https://orcid.org/0000-0003-4059-2891
Isabelle ArnulfParis Brain Institute (ICM), Sorbonne University, Inserm, CNRS, Paris, France.ORCID https://orcid.org/0000-0002-2240-2516
Delphine OudietteParis Brain Institute (ICM), Sorbonne University, Inserm, CNRS, Paris, France.ORCID https://orcid.org/0000-0002-6598-4130
Thomas AndrillonParis Brain Institute (ICM), Sorbonne University, Inserm, CNRS, Paris, France.ORCID https://orcid.org/0000-0003-2794-8494
INSIGHT‐preAD group

Funding

AvidFondation Recherche AlzheimerFoundation Plan-AlzheimerINSERMInvestissement d'Avenir ANR-10-AIHU-06Paris brain institute - Institut du Cerveau (ICM)Pfizer
6 · The paper itself

Abstract

introductionGrowing evidence supports a critical role of sleep slow waves (SW) in Alzheimer's disease (AD). However, wake SW (sleep-like SW potentially reflecting local intrusions of sleep) remain unexplored in AD.

methodsA total of 274 older adults with subjective cognitive decline (SCD) (INSIGHT-preAD cohort, 76.6 ± 3.5 years) underwent (i) positron emission tomography (PET) scans for amyloid (A) and neurodegeneration (N), (ii) high-density resting-state electroencephalogram (EEG) recordings to detect wake SW, and (iii) cognitive assessments. PET biomarkers were reassessed 2 years later. We examined wake SW associations with (1) current A/N status, (2) cognition, and (3) amyloid conversion.

resultsA+N-, A-N+, and A+N+ individuals exhibited lower delta wake SW density than A-N- participants. Wake SW amplitude (1) was higher in A+N+ than A-N- individuals, (2) correlated with poorer memory, and (3) predicted A- to A+ conversion (n = 157 A- stable individuals, n = 16 convertors). DISCUSSION: Wake SW represent promising early EEG biomarkers for AD pathology and amyloid conversion, facilitating risk stratification before cognitive decline onset.

Indexed as

Alzheimer DiseaseCognitive DysfunctionElectroencephalographySleep, Slow-WaveAgedAmyloid beta-PeptidesBiomarkersBrainFemaleHumansMaleNeuropsychological TestsPositron-Emission TomographyRestAmyloid beta-PeptidesBiomarkersAlzheimer's diseasebiomarkercognitionEEGSCDsleepslow waves

Identifiers

PMID42216470
PMCPMC13239585

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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.