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Related Experiment Videos

CNS dysfunction in the antiphospholipid syndrome.

A Katzav1, J Chapman, Y Shoenfeld

  • 1Department of Neurology, Sheba Medical Center, Tel Hashomer, Sackler Faculty of Medicine, Tel Aviv University, Israel.

Lupus
|January 13, 2004
PubMed
Summary
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Antiphospholipid syndrome (APS) causes neurological issues beyond stroke, including cognitive and behavioral changes. Animal models show promise for studying these APS manifestations and developing treatments.

Area of Science:

  • Neurology
  • Immunology
  • Pathophysiology

Background:

  • Antiphospholipid syndrome (APS) is characterized by neurological deficits, but only stroke is a diagnostic criterion.
  • Other neurological manifestations like dementia, epilepsy, and behavioral changes are associated with APS and antiphospholipid antibodies (aPL).

Purpose of the Study:

  • To review clinical data on neurological manifestations in APS.
  • To highlight the role of animal models in understanding APS-related neurological and behavioral deficits.
  • To explore potential therapeutic targets for cognitive and behavioral aspects of APS.

Main Methods:

  • Review of clinical case data for APS patients with neurological symptoms.
  • Utilizing mouse models immunized with beta2-glycoprotein I to induce aPL.

Related Experiment Videos

  • Employing models where patient IgG affects brain synaptoneurosomes.

    • Main Results:

    • Mouse models exhibit hyperactive behavior, learning, and memory deficits after beta2-glycoprotein I immunization.
    • Patient IgG has been shown to induce depolarization in brain synaptoneurosomes, modeling epilepsy.

    Conclusions:

    • Animal models, particularly those involving beta2-glycoprotein I and patient IgG, are valuable for studying APS neurological pathogenesis.
    • These models offer insights into cognitive, behavioral, and epilepsy aspects of APS, aiding future treatment development.