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Behavioral and cognitive deficits occur only after prolonged exposure of mice to antiphospholipid antibodies

A Katzav

Department of Physiology and Pharmacology, Sackler Faculty of Medicine, Tel Aviv University, Israel

A D Korczyn

Department of Physiology and Pharmacology, Tel Aviv University, Israel; Department of Neurology, Tel Aviv University, Israel; Sieratzki Chair of Neurology, Sackler Faculty of Medicine, Tel Aviv University, Israel

Y Litvinjuk

Department of Physiology and Pharmacology, Tel Aviv University, Israel; Abarbanel Mental Health Center, Bat Yam, Tel Aviv University, Israel

R Hershenson

Department of Physiology and Pharmacology, Sackler Faculty of Medicine, Tel Aviv University, Israel

C G Pick

Department of Anatomy, Sackler Faculty of Medicine, Tel Aviv University, Israel

M Blank

J Zaech

Y Shoenfeld

Department of Medicine B and Research Unit of Autoimmune Diseases, Sheba Medical Center, Tel Hashomer, Israel

P Sirota

Abarbanel Mental Health Center, Bat Yam, Sackler Faculty of Medicine, Tel Aviv University, Israel

J Chapman

Department of Physiology and Pharmacology, Tel Aviv University, Israel; Department of Neurology, Tel Aviv University, Israel

The antiphospholipid (Hughes) syndrome (APS) includes systemic and central nervous system (CNS) pathology associated with antibodies to a complex of phospholipids and ß₂-glycoprotein I (ß₂-GPI). ß₂-GPI immunized mice develop systemic manifestations of APS and we presently examined CNS manifestations in this APS model. Female BALB/c mice were immunized once with ß₂-GPI in complete Freund's adjuvant (CFA) or with CFA alone (controls). A staircase test and a T-maze alternation test were performed to test behavior and cognition in independent groups of mice 6, 12 and 18 weeks following the immunization. The APS mice developed elevated levels of antibodies against negatively charged phospholipids and ß₂-GPI. Neurological impairment was detected only 18 weeks after the induction of the APS and consisted of both cognitive (53± 4 71± 3% correct choices in the T-maze alternation for APS behavioral changes (higher number of rears (18± 2 vs 7±1, P < 0.02). This is the first report of cognitive deficits in this APS model and demonstrates the time course for the development of previously described behavioral changes. The mechanism involved in these CNS manifestations remains to be elucidated.

Key Words: antiphospholipid syndrome • animal model • behavior • ß2-glycoprotein I • memory

Lupus, Vol. 11, No. 11, 736-743 (2002)
DOI: 10.1191/0961203302lu255oa


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