Evidence map›Paper›PMID 29700007›Full record

ArticleBlood advances2018

Abnormal clotting of the intrinsic/contact pathway in Alzheimer disease patients is related to cognitive ability.

Georgette L Suidan, Pradeep K Singh, Sunita Patel-Hett, Zu-Lin Chen, Dmitri Volfson, Hitomi Yamamoto-Imoto, Erin H Norris, Robert D Bell, Sidney Strickland

Open access · goldAbstract read
In one paragraph

Article in Blood advances, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

25 citing papers in PubMed, 40 citations in OpenAlex.

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  20. Alzheimer's Disease and Vascular Aging: JACC Focus Seminar.Journal of the American College of Cardiology · 2020
    Review
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

9 authors at 3 institutions in 1 country.

Georgette L SuidanInternal Medicine Research Unit, Pfizer Inc., Cambridge, MA.
Pradeep K SinghPatricia and John Rosenwald Laboratory of Neurobiology and Genetics, Rockefeller University, New York, NY; and.
Sunita Patel-HettRare Disease Research Unit and.
Zu-Lin ChenPatricia and John Rosenwald Laboratory of Neurobiology and Genetics, Rockefeller University, New York, NY; and.
Dmitri VolfsonEarly Clinical Development, Pfizer Inc., Cambridge, MA.
Hitomi Yamamoto-ImotoPatricia and John Rosenwald Laboratory of Neurobiology and Genetics, Rockefeller University, New York, NY; and.
Erin H NorrisPatricia and John Rosenwald Laboratory of Neurobiology and Genetics, Rockefeller University, New York, NY; and.
Robert D BellRare Disease Research Unit and.
Sidney StricklandPatricia and John Rosenwald Laboratory of Neurobiology and Genetics, Rockefeller University, New York, NY; and.
Rockefeller University · USPfizer (United States) · USRare Disease Therapeutics (United States) · US

Funding

Role of the tPA/plasmin System in Alzheimers DiseaseR01NS050537 · NINDS · ROCKEFELLER UNIVERSITY · PI STRICKLAND, SIDNEY · 2004 to 2015
$5.7M
NINDS NIH HHS R01 NS050537
6 · The paper itself

Abstract

Alzheimer disease (AD) is a neurodegenerative disorder characterized by extracellular β-amyloid (Aβ) deposition. Although peripheral inflammation and cerebrovascular pathology are reported in AD, there is a lack of plasma biomarkers in this field. Because the contact system is triggered in patient plasma, we hypothesized that the hemostasis profile could be a novel biomarker in AD. Here, we assessed the clotting profile in plasma from AD patients and age-matched controls. Utilizing clinically relevant assays, thromboelastography and activated partial thromboplastin time, we found impaired clot initiation and formation rate in AD patient plasma. These coagulation end points correlated with cerebrospinal fluid neurofilament-light levels and cognition and were more profound in younger AD patients. Ex vivo intrinsic clotting of plasma from AD mice expressing human amyloid precursor protein (APP) was also delayed in an age-dependent manner, suggesting that this phenotype is related to APP, the parent protein of Aβ. Further analysis of coagulation factors in human plasma indicated that endogenous inhibitor(s) of factors XII and XI in AD plasma contribute to this delayed clotting. Together, these data suggest that delayed clotting in young AD patients is a novel biomarker and that therapies aimed to correct this phenotype might be beneficial in this patient population. Follow-up studies in additional AD patient cohorts are warranted to further evaluate these findings.

Indexed as

Blood CoagulationCognitionAgedAge FactorsAlzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsBiomarkersBlood Coagulation Factor InhibitorsHumansMaleMiceMice, TransgenicMiddle AgedPartial Thromboplastin TimeThrombelastographyAmyloid beta-Protein PrecursorAPP protein, humanBiomarkersBlood Coagulation Factor Inhibitors

Identifiers

PMID29700007
PMCPMC5942003
OpenAlexW2802324835

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.