Evidence map›Paper›PMID 37108211›Full record

ReviewInternational journal of molecular sciences2023

Vascular Dysfunction in Alzheimer's Disease: Alterations in the Plasma Contact and Fibrinolytic Systems.

Ana Badimon, Daniel Torrente, Erin H Norris

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Cross-platform proteomics signatures of extreme old age.bioRxiv : the preprint server for biology · 2024
    Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Fibrin-Targeting Immunotherapy for Dementia.The journal of prevention of Alzheimer's disease · 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

3 authors at 1 institution in 1 country.

Ana BadimonPatricia and John Rosenwald Laboratory of Neurobiology and Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.
Daniel TorrentePatricia and John Rosenwald Laboratory of Neurobiology and Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.
Erin H NorrisPatricia and John Rosenwald Laboratory of Neurobiology and Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.ORCID 0000-0002-4522-3537
Rockefeller University · US

Funding

Role of Fibrinogen in Alzheimer's DiseaseR01NS106668 · NINDS · ROCKEFELLER UNIVERSITY · PI Erin H. Norris, SIDNEY STRICKLAND · 2018 to 2026
$5.8M
Role of the Contact System in Alzheimer's DiseaseR01NS102721 · NINDS · ROCKEFELLER UNIVERSITY · PI Erin H. Norris, SIDNEY STRICKLAND · 2018 to 2026
$5.3M
Anti-high molecular weight kininogen antibody for Alzheimer's disease diagnosis and therapyRF1AG069987 · NIA · ROCKEFELLER UNIVERSITY · PI NORRIS, ERIN H · 2020 to 2020
$1.8M
NIA NIH HHS RF1 AG069987NINDS NIH HHS R01 NS102721NINDS NIH HHS R01 NS106668
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common neurodegenerative disease, affecting millions of people worldwide. The classical hallmarks of AD include extracellular beta-amyloid (Aβ) plaques and neurofibrillary tau tangles, although they are often accompanied by various vascular defects. These changes include damage to the vasculature, a decrease in cerebral blood flow, and accumulation of Aβ along vessels, among others. Vascular dysfunction begins early in disease pathogenesis and may contribute to disease progression and cognitive dysfunction. In addition, patients with AD exhibit alterations in the plasma contact system and the fibrinolytic system, two pathways in the blood that regulate clotting and inflammation. Here, we explain the clinical manifestations of vascular deficits in AD. Further, we describe how changes in plasma contact activation and the fibrinolytic system may contribute to vascular dysfunction, inflammation, coagulation, and cognitive impairment in AD. Given this evidence, we propose novel therapies that may, alone or in combination, ameliorate AD progression in patients.

Indexed as

Alzheimer DiseaseNeurodegenerative DiseasesAmyloid beta-PeptidesHumansInflammationNeurofibrillary TanglesAmyloid beta-PeptidesAlzheimer’s diseasebeta-amyloidcontact systemfibrinogenvasculature

Identifiers

PMID37108211
PMCPMC10138543
OpenAlexW4365147032

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.