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Maternal lupus and congenital cortical impairment - Bruce T. Volpe

March 27, 2012

Systemic lupus erythematosus (SLE) is an autoantibody (AAb)-mediated disease that preferentially affects women of childbearing age. Since the offspring of mothers with SLE exhibit a high frequency of learning disorders, we hypothesized that maternally transferred AAbs that bind DNA and the N-methyl-D-aspartate receptor (NMDAR) could play a pathogenic role during fetal brain development. Here we describe a maternal SLE murine model wherein pregnant dams harbored anti-DNA, anti-NMDAR AAbs throughout gestation. High titers of these AAbs in maternal circulation led to histopathological abnormalities in fetal brain and subsequent cognitive impairments in adult offspring. These data support a paradigm in which in utero exposure to neurotoxic AAbs causes abnormal brain development with long-term consequences. This paradigm may apply to multiple congenital neuropsychiatric disorders.

Studies demonstrate that children born to mothers with SLE display a high incidence of learning disorders compared to children born to healthy mothers1-5. In one study as many as 45% of the male and 8% of the female offspring of SLE mothers were affected, generally displaying dyslexia or difficulty with mathematical calculations1. The mechanisms for the learning disorder remain unknown, but prematurity, low birth weight, maternal disease activity, and medications during pregnancy have not emerged as significant causative factors. The striking observation that children born from SLE fathers do not exhibit learning disorders led us to ask whether maternally derived factors, antibodies (Abs) in particular, might alter fetal brain development in utero and result in long-term changes in cognitive function of the offspring.


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Source: Alliance for Lupus Research
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