Evidence map›Paper›PMID 25720414›Full record

ReviewJournal of Alzheimer's disease : JAD2015

Is Vasomotion in Cerebral Arteries Impaired in Alzheimer's Disease?

Luigi Yuri Di Marco, Eszter Farkas, Chris Martin, Annalena Venneri, Alejandro F Frangi

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of Alzheimer's disease : JAD, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

55 citing papers in PubMed, 94 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Vasomotion in Human Fingers.Journal of vascular research · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. High-resolution vasomotion analysis reveals novel arteriole physiological features and progressive modulation of cerebral vascular networks by stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
    Article
  15. Article
  16. Advancements in investigating the role of cerebral small vein loss in Alzheimer's disease-related pathological changes.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024
    Review
  17. Article
  18. Review
  19. Article
  20. APOE4 expression confers a mild, persistent reduction in neurovascular function in the visual cortex and hippocampus of awake mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023
    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

5 authors at 2 institutions in 3 countries.

Luigi Yuri Di MarcoCentre for Computational Imaging and Simulation Technologies in Biomedicine (CISTIB), Department of Electronic and Electrical Engineering, University of Sheffield, Sheffield, UK.
Eszter FarkasDepartment of Medical Physics and Informatics, Faculty of Medicine and Faculty of Science and Informatics, University of Szeged, Szeged, Hungary.
Chris MartinDepartment of Psychology, University of Sheffield, Sheffield, UK.
Annalena VenneriDepartment of Neuroscience, University of Sheffield, Sheffield, UK.
Alejandro F FrangiCentre for Computational Imaging and Simulation Technologies in Biomedicine (CISTIB), Department of Electronic and Electrical Engineering, University of Sheffield, Sheffield, UK.
University of Sheffield · GBUniversity of Szeged · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A substantial body of evidence supports the hypothesis of a vascular component in the pathogenesis of Alzheimer's disease (AD). Cerebral hypoperfusion and blood-brain barrier dysfunction have been indicated as key elements of this pathway. Cerebral amyloid angiopathy (CAA) is a cerebrovascular disorder, frequent in AD, characterized by the accumulation of amyloid-β (Aβ) peptide in cerebral blood vessel walls. CAA is associated with loss of vascular integrity, resulting in impaired regulation of cerebral circulation, and increased susceptibility to cerebral ischemia, microhemorrhages, and white matter damage. Vasomotion- the spontaneous rhythmic modulation of arterial diameter, typically observed in arteries/arterioles in various vascular beds including the brain- is thought to participate in tissue perfusion and oxygen delivery regulation. Vasomotion is impaired in adverse conditions such as hypoperfusion and hypoxia. The perivascular and glymphatic pathways of Aβ clearance are thought to be driven by the systolic pulse. Vasomotion produces diameter changes of comparable amplitude, however at lower rates, and could contribute to these mechanisms of Aβ clearance. In spite of potential clinical interest, studies addressing cerebral vasomotion in the context of AD/CAA are limited. This study reviews the current literature on vasomotion, and hypothesizes potential paths implicating impaired cerebral vasomotion in AD/CAA. Aβ and oxidative stress cause vascular tone dysregulation through direct effects on vascular cells, and indirect effects mediated by impaired neurovascular coupling. Vascular tone dysregulation is further aggravated by cholinergic deficit and results in depressed cerebrovascular reactivity and (possibly) impaired vasomotion, aggravating regional hypoperfusion and promoting further Aβ and oxidative stress accumulation.

Indexed as

Alzheimer DiseaseCerebral Arterial DiseasesCerebral ArteriesHumansVasomotor SystemAlzheimer’s diseasecerebral amyloid angiopathycerebral autoregulationendotheliumperivascular drainagevascular smooth muscle cellvasomotion

Identifiers

PMID25720414
PMCPMC4878307
OpenAlexW179558530

What OpenQuestion holds

Textmetadata
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.