Evidence map›Paper›PMID 39001629›Full record

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

Neurochemical organization of cortical proteinopathy and neurophysiology along the Alzheimer's disease continuum.

Alex I Wiesman, Jonathan Gallego-Rudolf, Sylvia Villeneuve, Sylvain Baillet, Tony W Wilson, PREVENT‐AD Research Group

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, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
–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 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Review
  4. Glial Cells in Behavioral and Psychological Symptoms of Alzheimer's Disease.International journal of molecular sciences · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. The PREVENT-AD cohort: Accelerating Alzheimer's disease research and treatment in Canada and beyond.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  10. Cortical Effects of Dopamine Replacement Account for Clinical Response Variability in Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2025
    Article
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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

6 authors.

Alex I WiesmanMcConnell Brain Imaging Centre, Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada.ORCID 0000-0003-0917-1570
Jonathan Gallego-RudolfMcConnell Brain Imaging Centre, Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada.
Sylvia VilleneuveMcConnell Brain Imaging Centre, Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada.
Sylvain BailletMcConnell Brain Imaging Centre, Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada.
Tony W WilsonInstitute for Human Neuroscience, Boys Town National Research Hospital, Omaha, Nebraska, USA.
PREVENT‐AD Research Group

Funding

Stress-Induced Aberrations in the Mitochondrial Redox Environment Impact Developing Neural Circuits Supporting Cognitive ControlP20GM144641 · NIGMS · FATHER FLANAGAN'S BOYS' HOME · PI Rachel K. Spooner · 2022 to 2026
$15.1M
BrainStorm: Highly Extensible Software for Advanced Electrophysiology and MEG/EEG ImagingR01EB026299 · NIBIB · UNIVERSITY OF SOUTHERN CALIFORNIA · PI LEAHY, RICHARD M · 2018 to 2025
$5.4M
MULTIMODAL IMAGING OF NEUROHIV DYNAMICS (MIND): AN OMAHA-PITTSBURGH CONSORTIUMR01MH118013 · NIMH · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI WILSON, TONY W · 2018 to 2022
$4.9M
THE PROGRESSIVE ELEVATION OF SPONTANEOUS CORTICAL ACTIVITY IN HAND (PESCAH) PROJECTR01MH116782 · NIMH · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI WILSON, TONY W · 2018 to 2022
$3.4M
Characterizing the interaction between neural attention and somato-motor systems in non-demented patients with Parkinson's diseaseF32NS119375 · NINDS · MCGILL UNIVERSITY · PI WIESMAN, ALEX I · 2020 to 2023
$205k
Alzheimer AssociationAlzheimer Society of CanadaBrain CanadaCanada Research ChairsCIHR 438655CIHR BPF-186555Healthy Brains Healthy Lives program at McGill UniversityMexican National Council of Science and Technology 2020-000017-02EXTF-00402Natural Sciences and Engineering Research Council of Canada RGPIN-2020-06889NIBIB NIH HHS R01 EB026299NIGMS NIH HHS P20 GM144641NIMH NIH HHS R01 MH116782NIMH NIH HHS R01 MH118013NINDS NIH HHS F32 NS119375United States National Institutes of Health F32-NS119375United States National Institutes of Health R01-EB026299United States National Institutes of Health R01-MH116782-S1United States National Institutes of Health R01-MH118013-S1
6 · The paper itself

Abstract

introductionDespite parallel research indicating amyloid-β accumulation, alterations in cortical neurophysiological signaling, and multi-system neurotransmitter disruptions in Alzheimer's disease (AD), the relationships between these phenomena remains unclear.

methodsUsing magnetoencephalography, positron emission tomography, and an atlas of 19 neurotransmitters, we studied the alignment between neurophysiological alterations, amyloid-β deposition, and the neurochemical gradients of the cortex.

resultsIn patients with mild cognitive impairment and AD, changes in cortical rhythms were topographically aligned with cholinergic, serotonergic, and dopaminergic systems. These alignments correlated with the severity of clinical impairments. Additionally, cortical amyloid-β plaques were preferentially deposited along neurochemical boundaries, influencing how neurophysiological alterations align with muscarinic acetylcholine receptors. Most of the amyloid-β-neurochemical and alpha-band neuro-physio-chemical alignments replicated in an independent dataset of individuals with asymptomatic amyloid-β accumulation. DISCUSSION: Our findings demonstrate that AD pathology aligns topographically with the cortical distribution of chemical neuromodulator systems and scales with clinical severity, with implications for potential pharmacotherapeutic pathways. HIGHLIGHTS: Changes in cortical rhythms in Alzheimer's are organized along neurochemical boundaries. The strength of these alignments is related to clinical symptom severity. Deposition of amyloid-β (Aβ) is aligned with similar neurotransmitter systems. Aβ deposition mediates the alignment of beta rhythms with cholinergic systems. Most alignments replicate in participants with pre-clinical Alzheimer's pathology.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesCerebral CortexMagnetoencephalographyPositron-Emission TomographyAgedAged, 80 and overCognitive DysfunctionFemaleHumansMaleNeurotransmitter AgentsPlaque, AmyloidAmyloid beta-PeptidesNeurotransmitter AgentsAlzheimer's disease continuumamyloid‐βmagnetoencephalographymild cognitive impairmentneural oscillationsneurotransmitter systemsrhythmic neurophysiological signalingspectral parameterization

Identifiers

PMID39001629
PMCPMC11497661

What OpenQuestion holds

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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.