Evidence map›Paper›PMID 41137705›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2025

Alzheimer's disease and its progression reduce pyramidal cell gain and connectivity.

Juliette H Lanskey, Amirhossein Jafarian, Melek Karadag, Ece Kocagoncu, Rebecca S Williams, Pranay Yadav, Andrew J Quinn, Jemma Pitt, Tony Thayanandan, Stephen Lowe and 8 more

Abstract read
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In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Alzheimer's disease and its progression reduce pyramidal cell gain and connectivity.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
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

18 authors.

Juliette H LanskeyMRC Cognition and Brain Sciences Unit, University of Cambridge, Cambridge, UK.
Amirhossein JafarianMRC Cognition and Brain Sciences Unit, University of Cambridge, Cambridge, UK.
Melek KaradagDepartment of Clinical Neurosciences and Cambridge University Hospitals NHS Foundation Trust, University of Cambridge, Cambridge, UK.
Ece KocagoncuDepartment of Clinical Neurosciences and Cambridge University Hospitals NHS Foundation Trust, University of Cambridge, Cambridge, UK.
Rebecca S WilliamsMRC Cognition and Brain Sciences Unit, University of Cambridge, Cambridge, UK.
Pranay YadavMRC Cognition and Brain Sciences Unit, University of Cambridge, Cambridge, UK.
Andrew J QuinnCentre for Human Brain Health, School of Psychology, University of Birmingham, Edgbaston, Birmingham, UK.
Jemma PittOxford Centre for Human Brain Activity, Wellcome Centre for Integrative Neuroimaging, Department of Psychiatry, University of Oxford, Oxford, UK.
Tony ThayanandanOxford Centre for Human Brain Activity, Wellcome Centre for Integrative Neuroimaging, Department of Psychiatry, University of Oxford, Oxford, UK.
Stephen LoweLilly Research Laboratories, Lilly Corporate Center, Indianapolis, Indiana, USA.
Michael PerkintonCambridge Biomedical Campus, Neuroscience, BioPharmaceuticals R&D, AstraZeneca, Cambridge, UK.
Maarten TimmersJanssen Pharmaceutica NV, a Johnson & Johnson Company, Beerse, Belgium.
Vanessa RaymontDepartment of Psychiatry, University of Oxford, Oxford, UK.
Krish D SinghSchool of Psychology, Cardiff University Brain Research Imaging Centre, Cardiff University, Cardiff, UK.
Mark WoolrichOxford Centre for Human Brain Activity, Wellcome Centre for Integrative Neuroimaging, Department of Psychiatry, University of Oxford, Oxford, UK.
Anna C NobreOxford Centre for Human Brain Activity, Wellcome Centre for Integrative Neuroimaging, Department of Psychiatry, University of Oxford, Oxford, UK.
Richard N HensonMRC Cognition and Brain Sciences Unit, University of Cambridge, Cambridge, UK.
James B RoweMRC Cognition and Brain Sciences Unit, University of Cambridge, Cambridge, UK.ORCID 0000-0001-7216-8679

Funding

Alzheimer's Research Trust ARUK-PG2017B-19Dementias Platform UKMedical Research Council MC_UU_00030/14Medical Research Council MR/T033371/1Medical Research Council SUAG/092 G116788Medical Research Council SUAG/096G116788NIHR Cambridge Biomedical Research Centre NIHR203312NIHR Oxford Health Biomedical Research Centre NIHR203316Wellcome TrustWellcome Trust 220258
6 · The paper itself

Abstract

introductionAlzheimer's disease (AD) affects neurophysiology by loss of neurons, synapses, and neurotransmitters. A mechanistic understanding of the human disease will facilitate new treatments.

methodsMagnetoencephalography was recorded during an auditory mismatch negativity paradigm from healthy adults (n = 14) and people with symptomatic AD (n = 45, amyloid biomarker positive) at baseline and after 16 months. Fourteen people with AD had repeat magnetoencephalography at 2 weeks to assess test-retest reliability. Dynamic causal models were fitted to the evoked responses and analyzed using parametric empirical Bayes.

resultsSensor data confirmed that AD and its progression reduce the mismatch negativity amplitude, which had excellent test-retest reliability. Parametric empirical Bayes analyses confirmed that AD progressively reduces extrinsic connectivity between pyramidal cells and superficial pyramidal cell gain modulation. DISCUSSION: Dynamic causal modeling revealed cellular-level causes of the neurophysiological deficits observed in AD. This approach may help facilitate experimental medicine studies of candidate treatments. HIGHLIGHTS: Magnetoencephalography scanning provides reliable biomarkers that are sensitive to Alzheimer's disease (AD) and its progression, and informative about disease mechanisms underlying cognitive decline. In vivo assays of pyramidal cell function during cognitive processes in humans improve our understanding of AD mechanisms. The amplitude of the mismatch negativity response is progressively reduced in AD. Reduced pyramidal cell gain and connectivity underlie this neurophysiological deficit. These measures are potential biomarkers for interventional studies.

Indexed as

Alzheimer DiseasePyramidal CellsAdultAgedBayes TheoremDisease ProgressionFemaleHumansMagnetoencephalographyMaleMiddle AgedReproducibility of Resultscanonical microcircuitconnectivitydementiadynamic causal modelingmagnetoencephalographymismatch negativity

Identifiers

PMID41137705
PMCPMC12553034

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Registered trials

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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.