Evidence map›Paper›PMID 36412244›Full record

ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2023

Gray matter hypoperfusion is a late pathological event in the course of Alzheimer's disease.

Khazar Ahmadi, Joana B Pereira, David Berron, Jacob Vogel, Silvia Ingala, Olof T Strandberg, Shorena Janelidze, Frederik Barkhof, Josef Pfeuffer, Linda Knutsson and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.5field-weighted citation impact, top 10% of its field
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

18 citing papers in PubMed, 22 citations in OpenAlex.

  1. Network-dependent remote effects and local tau burden jointly shape neuronal dysfunction in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Connectome-based predictive modeling of brain pathology and cognition in autosomal dominant Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  6. Article
  7. Cerebral hypoperfusion reduces tau accumulation.Annals of clinical and translational neurology · 2025
    Article
  8. Article
  9. Review
  10. Hypertension and cerebral blood flow in the development of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  11. Article
  12. Vascular contributions to cognitive decline: Beyond amyloid and tau in the Harvard Aging Brain Study.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
    Article
  13. Time-encoded ASL reveals lower cerebral blood flow in the early AD continuum.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
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

14 authors at 5 institutions in 5 countries.

Khazar AhmadiClinical Memory Research Unit, Department of Clinical Sciences, Lund University, Lund, Sweden.ORCID 0000-0002-3371-6211
Joana B PereiraClinical Memory Research Unit, Department of Clinical Sciences, Lund University, Lund, Sweden.
David BerronClinical Memory Research Unit, Department of Clinical Sciences, Lund University, Lund, Sweden.
Jacob VogelDepartment of Psychiatry, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Silvia IngalaDepartment of Radiology and Nuclear Medicine, Amsterdam University Medical Center, Location VUmc, Amsterdam Neuroscience, Amsterdam, the Netherlands.
Olof T StrandbergClinical Memory Research Unit, Department of Clinical Sciences, Lund University, Lund, Sweden.
Shorena JanelidzeClinical Memory Research Unit, Department of Clinical Sciences, Lund University, Lund, Sweden.
Frederik BarkhofDepartment of Radiology and Nuclear Medicine, Amsterdam University Medical Center, Location VUmc, Amsterdam Neuroscience, Amsterdam, the Netherlands.
Josef PfeufferApplication Development, Siemens Healthcare, Erlangen, Germany.ORCID 0000-0001-9887-0458
Linda KnutssonDepartment of Medical Radiation Physics, Lund University, Lund, Sweden.ORCID 0000-0002-4263-113X
Danielle van WestenClinical Memory Research Unit, Department of Clinical Sciences, Lund University, Lund, Sweden.
Sebastian PalmqvistClinical Memory Research Unit, Department of Clinical Sciences, Lund University, Lund, Sweden.
Henk Jmm MutsaertsDepartment of Radiology and Nuclear Medicine, Amsterdam University Medical Center, Location VUmc, Amsterdam Neuroscience, Amsterdam, the Netherlands.ORCID 0000-0003-0894-0307
Oskar HanssonClinical Memory Research Unit, Department of Clinical Sciences, Lund University, Lund, Sweden.
Lund University · SEAmsterdam Neuroscience · NLJohns Hopkins University · USSiemens Healthineers (Germany) · DEUniversity of Pennsylvania · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several studies have shown decreased cerebral blood flow (CBF) in Alzheimer's disease (AD). However, the role of hypoperfusion in the disease pathogenesis remains unclear. Combining arterial spin labeling MRI, PET, and CSF biomarkers, we investigated the associations between gray matter (GM)-CBF and the key mechanisms in AD including amyloid-β (Aβ) and tau pathology, synaptic and axonal degeneration. Further, we applied a disease progression modeling to characterize the temporal sequence of different AD biomarkers. Lower perfusion was observed in temporo-occipito-parietal cortex in the Aβ-positive cognitively impaired compared to both Aβ-negative and Aβ-positive cognitively unimpaired individuals. In participants along the AD spectrum, GM-CBF was associated with tau, synaptic and axonal dysfunction, but not Aβ in similar cortical regions. Axonal degeneration was further associated with hypoperfusion in cognitively unimpaired individuals. Disease progression modeling revealed that GM-CBF disruption Followed the abnormality of biomarkers of Aβ, tau and brain atrophy. These findings indicate that tau tangles and neurodegeneration are more closely connected with GM-CBF changes than Aβ pathology. Although subjected to the sensitivity of the employed neuroimaging techniques and the modeling approach, these findings suggest that hypoperfusion might not be an early event associated with the build-up of Aβ in preclinical phase of AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesBiomarkersDisease ProgressionGray MatterHumansAmyloid beta-PeptidesBiomarkersAlzheimer’s diseasearterial spin labelingcerebral blood flowneurodegenerationtau

Identifiers

PMID36412244
PMCPMC10063832
OpenAlexW4309654401

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.