Antiphospholipid syndrome induction exacerbates a transgenic Alzheimer disease model on a female background

Aviva Katzav, Achinoam Faust-Socher, Filip Kvapil, Daniel M. Michaelson, Miri Blank, Chaim G. Pick, Yehuda Shoenfeld, Amos D. Korczyn, Joab Chapman

Research output: Contribution to journalArticlepeer-review

Abstract

The antiphospholipid syndrome (APS) is characterized by antiphospholipid antibodies (aPL) and vascular brain disease which is often associated with dementia. We examined the neurodegenerative pathological processes underlying APS by inducing APS in a transgenic animal model of Alzheimer's disease. Female C57B6/SJL mice carrying the APP695SWE mutation (Tg2576) and wild-type (wt) controls were immunized with β2-glycoprotein-I (APS mice) or adjuvant alone (controls) at 4 months of age. At the age of 8 months the APP-APS mice developed high levels of aPL associated with motor hypoactivity in a staircase test (p<0.03 by t-test) and impaired performance in the cognitive T-maze (p<0.02 for main effect of treatment by repeated measures ANOVA) relative to APP-CFA mice and controls. wt-APS and wt-control did not differ significantly in their behavior or cognition. Histological studies revealed mature plaques only in the APP-APS group which also had higher amyloid load and number of activated microglia compared to all other groups. The results indicate a significant interaction between APP genotype and the induction of APS on a female background. The mechanisms involved may also be important in human APS-AD co-morbidity.

Original languageEnglish
Pages (from-to)272-279
Number of pages8
JournalNeurobiology of Aging
Volume32
Issue number2
DOIs
StatePublished - Feb 2011

Keywords

  • Activated microglia
  • Alzheimer's disease
  • Amyloid plaque
  • Amyloid precursor protein
  • Antiphospholipid syndrome
  • Behavior
  • Cognition
  • Transgenic mouse

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