Evidence map›Paper›PMID 24741580›Full record

ReviewJournal of immunology research2014

Revisiting the molecular mechanism of neurological manifestations in antiphospholipid syndrome: beyond vascular damage.

M Carecchio, R Cantello, C Comi

Open access · goldAbstract readReview
In one paragraph

Review in Journal of immunology research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

21 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. Article
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  7. Review
  8. β2 glycoprotein I participates in phagocytosis of apoptotic neurons and in vascular injury in experimental brain stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
    Article
  9. Review
  10. Article
  11. Stroke presenting with an isolated foot drop in a patient with antiphospholipid syndrome: an uncommon clinical entity.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2019
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Immunotherapies for Neurological Manifestations in the Context of Systemic Autoimmunity.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2016
    Review
  17. Review
  18. Article
  19. 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 1 institution in 1 country.

M CarecchioSection of Neurology, Department of Translational Medicine, University of Eastern Piedmont, "Amedeo Avogadro", Via Solaroli 17, 28100 Novara, Italy.
R CantelloSection of Neurology, Department of Translational Medicine, University of Eastern Piedmont, "Amedeo Avogadro", Via Solaroli 17, 28100 Novara, Italy.
C ComiSection of Neurology, Department of Translational Medicine, University of Eastern Piedmont, "Amedeo Avogadro", Via Solaroli 17, 28100 Novara, Italy ; Interdisciplinary Research Center of Autoimmune Diseases (IRCAD), University of Eastern Piedmont, "Amedeo Avogadro", Via Solaroli 17, 28100 Novara, Italy.
Università degli Studi del Piemonte Orientale “Amedeo Avogadro” · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Antiphospholipid syndrome (APS) is a multiorgan disease often affecting the central nervous system (CNS). Typically, neurological manifestations of APS include thrombosis of cerebral vessels leading to stroke and requiring prompt initiation of treatment with antiplatelet drugs or anticoagulant therapy. In these cases, alterations of the coagulation system at various levels caused by multiple effects of antiphospholipid antibodies (aPL) have been postulated to explain the vascular damage to the CNS in APS. However, several nonvascular neurological manifestations of APS have progressively emerged over the past years. Nonthrombotic, immune-mediated mechanisms altering physiological basal ganglia function have been recently suggested to play a central role in the pathogenesis of these manifestations that include, among others, movement disorders such as chorea and behavioral and cognitive alterations. Similar clinical manifestations have been described in other autoimmune CNS diseases such as anti-NMDAR and anti-VGCK encephalitis, suggesting that the spectrum of immune-mediated basal ganglia disorders is expanding, possibly sharing some pathophysiological mechanisms. In this review, we will focus on thrombotic and nonthrombotic neurological manifestations of APS with particular attention to immune-mediated actions of aPL on the vascular system and the basal ganglia.

Indexed as

Antiphospholipid SyndromeHumansThrombosis

Identifiers

PMID24741580
PMCPMC3987798
OpenAlexW2021422415

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.