Evidence map›Paper›PMID 20388225›Full record

ArticleMolecular neurodegeneration2010

Soluble amyloid-beta, effect on cerebral arteriolar regulation and vascular cells.

Hans H Dietrich, Chuanxi Xiang, Byung H Han, Gregory J Zipfel, David M Holtzman

Open access · goldAbstract read
In one paragraph

Article in Molecular neurodegeneration, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

46 citing papers in PubMed, 78 citations in OpenAlex.

  1. Endothelial NADAlzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  2. Amyloid β alters vascular CaThe Journal of physiology · 2025
    Article
  3. AβInternational journal of molecular sciences · 2025
    Article
  4. Observational
  5. Review
  6. Article
  7. Article
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  9. Article
  10. Article
  11. Article
  12. Article
  13. Vascular contributions to Alzheimer's disease.Translational research : the journal of laboratory and clinical medicine · 2023
    Review
  14. Article
  15. Cerebral vasomotor reactivity across the continuum of subjective cognitive impairment, amnestic mild cognitive impairment and probable Alzheimer's dementia: A transcranial Doppler and PET/MRI study.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023
    Article
  16. Review
  17. Article
  18. Review
  19. Causes and consequences of baseline cerebral blood flow reductions in Alzheimer's disease.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
    Review
  20. Ferulic Acid Ameliorates Alzheimer's Disease-like Pathology and Repairs Cognitive Decline by Preventing Capillary Hypofunction in APP/PS1 Mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021
    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 3 institutions in 1 country.

Hans H DietrichDepartment of Neurological Surgery, Hope Center for Neurological Disorders, and Alzheimer's Disease Research Center, Washington University School of Medicine, St Louis, MO, 63110, USA. DietrichH@nsurg.wustl.edu.
Chuanxi Xiang
Byung H Han
Gregory J Zipfel
David M Holtzman
Neurological Surgery · USHope Center for Neurological Disorders · USWashington University in St. Louis · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEvidence indicates that soluble forms of amyloid-beta (Abeta) are vasoactive, which may contribute to cerebrovascular dysfunction noted in patients with Alzheimer's Disease and cerebral amyloid angiopathy. The effects of soluble Abeta on penetrating cerebral arterioles - the vessels most responsible for controlling cerebrovascular resistance - have not been studied.

resultsFreshly dissolved Abeta1-40 and Abeta1-42, but not the reverse peptide Abeta40-1 constricted isolated rat penetrating arterioles and diminished dilation to adenosine tri-phosphate (ATP). Abeta1-42 also enhanced ATP-induced vessel constriction. Abeta1-40 diminished arteriolar myogenic response, and an anti-Abeta antibody reduced Abeta1-40 induced arteriolar constriction. Prolonged Abeta exposure in vessels of Tg2576 mice resulted in a marked age-dependent effect on ATP-induced vascular responses. Vessels from 6 month old Tg2576 mice had reduced vascular responses whereas these were absent from 12 month old animals. Abeta1-40 and Abeta1-42 acutely increased production of reactive oxygen species (ROS) in cultured rat cerebro-microvascular cells. The radical scavenger MnTBAP attenuated this Abeta-induced oxidative stress and Abeta1-40-induced constriction in rat arterioles.

conclusionsOur results suggest that soluble Abeta1-40 and Abeta1-42 directly affect the vasomotor regulation of isolated rodent penetrating arterioles, and that ROS partially mediate these effects. Once insoluble Abeta deposits are present, arteriolar reactivity is greatly diminished.

Identifiers

PMID20388225
PMCPMC2873254
OpenAlexW2146597523

What OpenQuestion holds

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LicenceCC BY
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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.