Evidence map›Paper›PMID 22869464›Full record

ReviewJournal of Alzheimer's disease : JAD2012

Fibrinogen and altered hemostasis in Alzheimer's disease.

Marta Cortes-Canteli, Daria Zamolodchikov, Hyung Jin Ahn, Sidney Strickland, Erin H Norris

Abstract readReview
In one paragraph

Review in Journal of Alzheimer's disease : JAD, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

93 citing papers in PubMed, 182 citations in OpenAlex.

  1. Review
  2. Unveiling the procoagulant state in Alzheimer's disease: A novel PET imaging strategy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

33 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Marta Cortes-CanteliLaboratory of Neurobiology and Genetics, The Rockefeller University, New York, NY 10065, USA.
Daria Zamolodchikov
Hyung Jin Ahn
Sidney Strickland
Erin H Norris
Rockefeller University · US

Funding

WASHINGTON UNIVERSITY ALZHEIMERS DISEASE RESEARCH CENTERP50AG005681 · NIA · WASHINGTON UNIVERSITY · PI MORRIS, JOHN · 1985 to 2019
$52.1M
A Natonal Resource for Postmortem Brain ResearchR24MH068855 · NIMH · MC LEAN HOSPITAL (BELMONT, MA) · PI BENES, FRANCINE M. · 2003 to 2012
$14.8M
Role of the tPA/plasmin System in Alzheimers DiseaseR01NS050537 · NINDS · ROCKEFELLER UNIVERSITY · PI STRICKLAND, SIDNEY · 2004 to 2015
$5.7M
NIA NIH HHS P50 AG005681NIA NIH HHS P50 AG05681NIMH NIH HHS R24 MH068855NIMH NIH HHS R24-MH 068855NINDS NIH HHS NS050537NINDS NIH HHS R01 NS050537
6 · The paper itself

Abstract

Alzheimer's disease (AD) is characterized by amyloid-β (Aβ) plaques, tau tangles, brain atrophy, and vascular pathology. Vascular defects include cerebrovascular dysfunction, decreased cerebral blood flow, and blood brain barrier (BBB) disruption, among others. Here, we review the evidence that links Aβ with the vascular pathology present in AD, with a specific focus on the hemostatic system and the clotting protein fibrinogen. Fibrinogen is normally found circulating in blood, but in AD it deposits with Aβ in the brain parenchyma and cerebral blood vessels. We found that Aβ and fibrin(ogen) interact, and their binding leads to increased fibrinogen aggregation, Aβ fibrillization, and the formation of degradation-resistant fibrin clots. Decreasing fibrinogen levels not only lessens cerebral amyloid angiopathy and BBB permeability, but it also reduces microglial activation and improves cognitive performance in AD mouse models. Moreover, a prothrombotic state in AD is evidenced by increased clot formation, decreased fibrinolysis, and elevated levels of coagulation factors and activated platelets. Abnormal deposition and persistence of fibrin(ogen) in AD may result from Aβ-fibrin(ogen) binding and altered hemostasis and could thus contribute to Aβ deposition, decreased cerebral blood flow, exacerbated neuroinflammation, and eventual neurodegeneration. Blocking the interaction between fibrin(ogen) and Aβ may be a promising therapeutic target for AD.

Indexed as

Alzheimer DiseaseAnimalsBlood-Brain BarrierCerebrovascular CirculationFibrinogenHemostasisHumansFibrinogen

Identifiers

PMID22869464
PMCPMC3683985
OpenAlexW1538828624

What OpenQuestion holds

Textmetadata
LicenceTDM
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.