Neurological dysfunction and hyperactive behavior associated with antiphospholipid antibodies a mouse model

Lea Ziporen, Yehuda Shoenfeld*, Yair Levy, Amos D. Korczyn

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

Abstract

Antiphospholipid antibodies (aPL) have been associated with various neurological manifestations, but the underlying mechanism has not been elucidated. We assessed mice with induced experimental antiphospholipid syndrome (APS) for neurological and behavioral changes. After immunization with monoclonal human anticardiolipin antibody (H-3), female BALB/c mice developed elevated levels of circulating anti-negatively charged phospholipids (aPL), anti-β2-glycoprotein I (aβ2GPI), and anti- endothelial cell antibodies (AECA), along with clinical manifestations of APS like thrombocytopenia and fetus resorption. APS mice were impaired neurologically and performed several reflexes less accurately compared to the controls, including placing reflex (P < 0.05), postural reflex (P < 0.05), and grip test (P = 0.05). The APS mice also exhibited hyperactive behavior in an open field, which tests spatial behavior (P < 0.03), and displayed impaired motor coordination on a rotating bar. aPL in combination with aβ2GPI and AECA is probably involved in the neurological and behavioral defects shown in mice with experimental APS.

Original languageEnglish
Pages (from-to)613-619
Number of pages7
JournalJournal of Clinical Investigation
Volume100
Issue number3
DOIs
StatePublished - 1 Aug 1997

Keywords

  • Anticardiolipin antibodies
  • Antiphospholipid syndrome
  • Autoimmune experimental model
  • Autoimmunity
  • Behavioral defects

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