Evidence map›Paper›PMID 39754275›Full record

ArticleAlzheimer's research & therapy2025

The cerebral blood flow response to neuroactivation is reduced in cognitively normal men with β-amyloid accumulation.

Mark Bitsch Vestergaard, Aftab Bakhtiari, Merete Osler, Erik Lykke Mortensen, Ulrich Lindberg, Ian Law, Martin Lauritzen, Krisztina Benedek, Henrik Bo Wiberg Larsson

Abstract read
In one paragraph

Article in Alzheimer's research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Review
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  3. Article
  4. Article
  5. Glymphatic and meningeal lymphatic dysfunction in Alzheimer's disease: Mechanisms and therapeutic perspectives.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  6. Review
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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

9 authors.

Mark Bitsch VestergaardFunctional Imaging Unit, Department of Clinical Physiology and Nuclear Medicine, Copenhagen University Hospital Rigshospitalet, Valdemar Hansens Vej 1-23, Glostrup, 2600, Denmark. Mark.bitsch.vestergaard@regionh.dk.
Aftab BakhtiariFunctional Imaging Unit, Department of Clinical Physiology and Nuclear Medicine, Copenhagen University Hospital Rigshospitalet, Valdemar Hansens Vej 1-23, Glostrup, 2600, Denmark.
Merete OslerCenter for Clinical Research and Prevention, Copenhagen University Hospital Bispebjerg and Frederiksberg, Copenhagen, Denmark.
Erik Lykke MortensenDepartment of Public Health, University of Copenhagen, Copenhagen, Denmark.
Ulrich LindbergFunctional Imaging Unit, Department of Clinical Physiology and Nuclear Medicine, Copenhagen University Hospital Rigshospitalet, Valdemar Hansens Vej 1-23, Glostrup, 2600, Denmark.
Ian LawDepartment of Clinical Physiology and Nuclear Medicine, Copenhagen University Hospital Rigshospitalet, Copenhagen, Denmark.
Martin LauritzenDepartment of Clinical Neurophysiology, Copenhagen University Hospital Rigshospitalet, Glostrup, Denmark.
Krisztina BenedekDepartment of Clinical Neurophysiology, Copenhagen University Hospital Rigshospitalet, Glostrup, Denmark.
Henrik Bo Wiberg LarssonFunctional Imaging Unit, Department of Clinical Physiology and Nuclear Medicine, Copenhagen University Hospital Rigshospitalet, Valdemar Hansens Vej 1-23, Glostrup, 2600, Denmark.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAccumulation of β-amyloid (Aβ) in the brain is a hallmark of Alzheimer's Disease (AD). Cerebral deposition of Aβ initiates deteriorating pathways which eventually can lead to AD. However, the exact mechanisms are not known. A possible pathway could be that Aβ affects the cerebral vessels, causing inadequate cerebrovascular function. In the present study, we examined if Aβ accumulation is associated with a reduced cerebral blood flow response (CBF) to neuronal activation by visual stimulation (ΔCBF

methods64 subjects participated in the present study. ΔCBF

resultsΔCBF

conclusionWe found a correlation between high PiB SUVr and reduced CBF response to neuronal activation, indicating a link between Aβ accumulation and impaired cerebrovascular function. The impairment was not associated with cortical thinning or hypometabolism, suggesting that Aβ accumulation affecting brain vessel function could be a very early pathology leading to neurodegenerative disease.

Indexed as

Amyloid beta-PeptidesBrainCerebrovascular CirculationMagnetic Resonance ImagingPositron-Emission TomographyThiazolesAniline CompoundsCohort StudiesFluorodeoxyglucose F18HumansMaleMiddle AgedPhotic Stimulation2-(4'-(methylamino)phenyl)-6-hydroxybenzothiazoleAmyloid beta-PeptidesAniline CompoundsFluorodeoxyglucose F18ThiazolesAgingAlzheimer’s diseaseCerebral blood flowCerebrovascular functionCerebrovascular reactivityNeurovascular couplingPiB PETβ-amyloid

Identifiers

PMID39754275
PMCPMC11699738

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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.