Evidence map›Paper›PMID 39254209›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2024

Amygdala atrophies in specific subnuclei in preclinical Alzheimer's disease.

Yasmine Salman, Thomas Gérard, Lara Huyghe, Lise Colmant, Lisa Quenon, Vincent Malotaux, Adrian Ivanoiu, Renaud Lhommel, Laurence Dricot, Bernard J Hanseeuw and 1 more

Abstract read
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Article
  2. Review
  3. The Amygdala and Politics.Brain sciences · 2026
    Review
  4. Review
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  16. Amygdala atrophies in specific subnuclei in preclinical Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    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

11 authors.

Yasmine SalmanLouvain Aging Brain Lab, Institute of Neuroscience, UCLouvain, Brussels, Belgium.ORCID 0000-0002-8564-5136
Thomas GérardLouvain Aging Brain Lab, Institute of Neuroscience, UCLouvain, Brussels, Belgium.ORCID 0000-0001-7997-3945
Lara HuygheLouvain Aging Brain Lab, Institute of Neuroscience, UCLouvain, Brussels, Belgium.ORCID 0009-0009-3568-3474
Lise ColmantLouvain Aging Brain Lab, Institute of Neuroscience, UCLouvain, Brussels, Belgium.ORCID 0009-0006-6511-0819
Lisa QuenonLouvain Aging Brain Lab, Institute of Neuroscience, UCLouvain, Brussels, Belgium.ORCID 0000-0001-9139-2422
Vincent MalotauxLouvain Aging Brain Lab, Institute of Neuroscience, UCLouvain, Brussels, Belgium.ORCID 0000-0003-0737-9220
Adrian IvanoiuNeurology Department, Saint-Luc University Hospital, Brussels, Belgium.
Renaud LhommelNuclear Medicine Department, Saint-Luc University Hospital, Brussels, Belgium.ORCID 0000-0003-0668-6122
Laurence DricotLouvain Aging Brain Lab, Institute of Neuroscience, UCLouvain, Brussels, Belgium.ORCID 0000-0002-8613-2420
Bernard J HanseeuwLouvain Aging Brain Lab, Institute of Neuroscience, UCLouvain, Brussels, Belgium.ORCID 0000-0002-3102-6778
Alzheimer's Disease Neuroimaging Initiative

Funding

Alzheimer's Disease Neuroimaging Initiative - SupplementU01AG024904 · NIA · NORTHERN CALIFORNIA INSTITUTE RES &EDUC · PI WEINER, MICHAEL W · 2004 to 2015
$121.0M
Human White Matter Tract Mapping by Diffusion MRIR01AG020012 · NIA · JOHNS HOPKINS UNIVERSITY · PI MORI, SUSUMU · 2001 to 2011
$4.1M
AbbVieAlzheimer's AssociationAlzheimer's Disease Neuroimaging Initiative (ADNI) W81XWH-12-2-0012Alzheimer's Drug Discovery FoundationAlzheimer's Therapeutic Research Institute at the University of Southern CaliforniaAraclon BiotechBelgian Alzheimer Research FoundationBelgian Fund for Scientific Research (FNRS) CCL40010417Belgian Fund for Scientific Research (FNRS) FRIA40014635BioClinica, IncBiogenBristol-Myers Squibb CompanyCereSpir, IncCIHRCogstateDepartment of DefenseEisai Inc.Elan Pharmaceuticals, Inc.Eli Lilly and CompanyEuroImmunF. Hoffmann-La Roche LtdFRFS-WELBIO 40010035GE HealthcareGenentech, Inc.IXICO LtdJanssen Alzheimer Immunotherapy Research & Development, LLC.Johnson & Johnson Pharmaceutical Research & Development LLCLaboratory for Neuro Imaging at the University of Southern CaliforniaLumosityMerck & Co., Inc.Meso Scale Diagnostics, LLC.NeuroRx ResearchNeurotrack TechnologiesNIA NIH HHS U01 AG024904NIBIB NIH HHSNIH HHSNorthern California Institute for Research and EducationNovartis Pharmaceuticals CorporationPfizer Inc.Piramal ImagingServierTakeda Pharmaceutical CompanyTransition Therapeutics
6 · The paper itself

Abstract

introductionMagnetic resonance imaging (MRI) segmentation algorithms make it possible to study detailed medial temporal lobe (MTL) substructures as hippocampal subfields and amygdala subnuclei, offering opportunities to develop biomarkers for preclinical Alzheimer's disease (AD).

methodsWe identified the MTL substructures significantly associated with tau-positron emission tomography (PET) signal in 581 non-demented individuals from the Alzheimer's Disease Neuroimaging Initiative (ADNI-3). We confirmed our results in our UCLouvain cohort including 110 non-demented individuals by comparing volumes between individuals with different visual Braak's stages and clinical diagnosis.

resultsFour amygdala subnuclei (cortical, central, medial, and accessory basal) were associated with tau in amyloid beta-positive (Aβ+) clinically normal (CN) individuals, while the global amygdala and hippocampal volumes were not. Using UCLouvain data, we observed that both Braak I-II and Aβ+ CN individuals had smaller volumes in these subnuclei, while no significant difference was observed in the global structure volumes or other subfields.

conclusionMeasuring specific amygdala subnuclei, early atrophy may serve as a marker of temporal tauopathy in preclinical AD, identifying individuals at risk of progression. HIGHLIGHTS: Amygdala atrophy is not homogeneous in preclinical Alzheimer's disease (AD). Tau pathology is associated with atrophy of specific amygdala subnuclei, specifically, the central, medial, cortical, and accessory basal subnuclei. Hippocampal and amygdala volume is not associated with tau in preclinical AD. Hippocampus and CA1-3 volume is reduced in preclinical AD, regardless of tau.

Indexed as

Alzheimer DiseaseAmygdalaAtrophyMagnetic Resonance ImagingPositron-Emission Tomographytau ProteinsAgedAged, 80 and overAmyloid beta-PeptidesBiomarkersFemaleHippocampusHumansMaleNeuroimagingTemporal LobeAmyloid beta-PeptidesBiomarkerstau ProteinsAlzheimer's diseaseamygdala subnucleiAV1451biomarkerflorquinitauflortaucipirMK6240preclinical ADstructural magnetic resonance imagingtauopathytau‐positron emission tomography

Identifiers

PMID39254209
PMCPMC11485073

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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.