Evidence map›Paper›PMID 22415062›Full record

ArticleJournal of neural transmission (Vienna, Austria : 1996)2012

Plasmin system of Alzheimer's disease patients: CSF analysis.

Alessandro Martorana, Giulia M Sancesario, Zaira Esposito, Marzia Nuccetelli, Roberto Sorge, Amanda Formosa, Vincenzo Dinallo, Giorgio Bernardi, Sergio Bernardini, Giuseppe Sancesario

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of neural transmission (Vienna, Austria : 1996), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

12 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Hemostasis components in cerebral amyloid angiopathy and Alzheimer's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Cerebrospinal fluid biomarkers of neurovascular dysfunction in mild dementia and Alzheimer's disease.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2015
    Review
  12. 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

10 authors at 3 institutions in 1 country.

Alessandro MartoranaDepartment of Neuroscience, University of Rome Tor Vergata, 1 Montpellier Street, 00133, Rome, Italy. martorana@med.uniroma2.it
Giulia M Sancesario
Zaira Esposito
Marzia Nuccetelli
Roberto Sorge
Amanda Formosa
Vincenzo Dinallo
Giorgio Bernardi
Sergio Bernardini
Giuseppe Sancesario
University of Rome Tor Vergata · ITFondazione Santa Lucia · ITIstituti di Ricovero e Cura a Carattere Scientifico · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder characterized by the extracellular deposit of Amyloid beta (Aβ), mainly of the Amyloid beta(1-42) (Aβ(1-42)) peptide in the hippocampus and neocortex leading to progressive cognitive decline and dementia. The possible imbalance between the Aβ production/degradation process was suggested to contribute to the pathogenesis of AD. Among others, the serine protease plasmin has shown to be involved in Aβ(1-42) clearance, a hypothesis strengthened by neuropathological studies on AD brains. To explore whether there is a change in plasmin system in CSF of AD patients, we analyzed CSF samples from AD and age-matched controls, looking at plasminogen, tissue plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI-1) protein levels and t-PA and urokinase plasminogen activator (u-PA) enzymatic activities. We also measured Aβ(1-42), total-tau and phospho-tau (181) CSF levels and sought for a possible relationship between them and plasmin system values. Our findings showed that t-PA, plasminogen and PAI-1 levels, as t-PA enzymatic activity, remained unchanged in AD with respect to controls; u-PA activity was not detected. We conclude that CSF analysis of plasminogen system does not reflect changes observed post-mortem. Unfortunately, the CSF detection of plasmin system could not be a useful biomarker for either AD diagnosis or disease progression. However, these findings do not exclude the possible involvement of the plasmin system in AD.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseAmyloid beta-PeptidesBiomarkersFemaleFibrinolysinHumansMaleMiddle AgedNeuropsychological TestsPeptide FragmentsPhosphorylationPlasminogenPlasminogen Activator Inhibitor 1tau ProteinsAmyloid beta-Peptidesamyloid beta-protein (1-42)BiomarkersFibrinolysinPeptide FragmentsPlasminogenPlasminogen Activator Inhibitor 1tau ProteinsTissue Plasminogen ActivatorUrokinase-Type Plasminogen Activator

Identifiers

PMID22415062
OpenAlexW2010472460

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.