Evidence map›Paper›PMID 32183293›Full record

ReviewInternational journal of molecular sciences2020

Potential Role of Venular Amyloid in Alzheimer's Disease Pathogenesis.

Christopher D Morrone, Jossana Bishay, JoAnne McLaurin

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.5field-weighted citation impact, top 8% 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

28 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. 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
  9. Super-Resolution Ultrasound Reveals Cerebrovascular Impairment in a Mouse Model of Alzheimer's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  10. Article
  11. Review
  12. Review
  13. Cerebral venous congestion alters brain metabolite profiles, impairing cognitive function.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023
    Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Deep medullary veins are associated with widespread brain structural abnormalities.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022
    Article
  20. 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

3 authors at 2 institutions in 1 country.

Christopher D MorroneSunnybrook Research Institute, Biological Sciences, 2075 Bayview Ave, Toronto, ON M4N 3M5, Canada.
Jossana BishaySunnybrook Research Institute, Biological Sciences, 2075 Bayview Ave, Toronto, ON M4N 3M5, Canada.
JoAnne McLaurinSunnybrook Research Institute, Biological Sciences, 2075 Bayview Ave, Toronto, ON M4N 3M5, Canada.
University of New Brunswick · CASunnybrook Health Science Centre · CA

Funding

Canada Research Chairs Program and National Institutes of Health R01 AG057665-02CIHR PJY153101
6 · The paper itself

Abstract

Insurmountable evidence has demonstrated a strong association between Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA), along with various other cerebrovascular diseases. One form of CAA, which is the accumulation of amyloid-beta peptides (Aβ) along cerebral vessel walls, impairs perivascular drainage pathways and contributes to cerebrovascular dysfunction in AD. To date, CAA research has been primarily focused on arterial Aβ, while the accumulation of Aβ in veins and venules were to a lesser extent. In this review, we describe preclinical models and clinical studies supporting the presence of venular amyloid and potential downstream pathological mechanisms that affect the cerebrovasculature in AD. Venous collagenosis, impaired cerebrovascular pulsatility, and enlarged perivascular spaces are exacerbated by venular amyloid and increase Aβ deposition, potentially through impaired perivascular clearance. Gaining a comprehensive understanding of the mechanisms involved in venular Aβ deposition and associated pathologies will give insight to how CAA contributes to AD and its association with AD-related cerebrovascular disease. Lastly, we suggest that special consideration should be made to develop Aβ-targeted therapeutics that remove vascular amyloid and address cerebrovascular dysfunction in AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloidogenic ProteinsBrainCerebral Amyloid AngiopathyHumansPlaque, AmyloidVenous InsufficiencyVenulesAmyloid beta-PeptidesAmyloidogenic ProteinsAlzheimer’s diseaseAβcerebral amyloid angiopathyperivascular clearanceTgF344-AD rat modelvein/venulevenous collagenosisvenular amyloid

Identifiers

PMID32183293
PMCPMC7139584
OpenAlexW3012145010

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.