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Neurological dysfunction and hyperactive behavior associated with antiphospholipid antibodies. A mouse model

L Ziporen1, Y Shoenfeld, Y Levy

  • 1Research Unit of Autoimmune Diseases, Department of Medicine B, Sheba Medical Center, Tel-Hashomer, Israel.

The Journal of Clinical Investigation
|August 1, 1997
PubMed
Summary
This summary is machine-generated.

Antiphospholipid antibodies (aPL) cause neurological and behavioral deficits in mice with experimental antiphospholipid syndrome (APS). These findings suggest aPL, anti-beta2-glycoprotein I, and anti-endothelial cell antibodies contribute to APS-related neurological issues.

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Area of Science:

  • Neuroimmunology
  • Autoimmunity
  • Animal Models

Background:

  • Antiphospholipid antibodies (aPL) are linked to neurological symptoms, but mechanisms remain unclear.
  • Experimental antiphospholipid syndrome (APS) provides a model to study these neurological effects.

Purpose of the Study:

  • To investigate neurological and behavioral changes in mice with experimentally induced APS.
  • To explore the role of specific antibodies in APS-related neurological dysfunction.

Main Methods:

  • Female BALB/c mice were immunized to induce experimental APS.
  • Neurological reflexes, motor coordination, and behavior (open field test) were assessed.
  • Circulating antibody levels (aPL, anti-beta2-glycoprotein I, AECA) were measured.

Main Results:

  • APS mice showed impaired placing and postural reflexes, and grip tests.
  • Hyperactivity in the open field test and impaired motor coordination were observed in APS mice.
  • Elevated aPL, anti-beta2-glycoprotein I, and AECA levels correlated with neurological and behavioral deficits.

Conclusions:

  • Experimental APS in mice leads to significant neurological and behavioral impairments.
  • The combination of aPL, anti-beta2-glycoprotein I, and AECA likely contributes to the observed neurological defects in APS.