Cognitive and emotional abnormalities in systemic lupus erythematosus: evidence for amygdala dysfunction - PubMed (original) (raw)

Review

Cognitive and emotional abnormalities in systemic lupus erythematosus: evidence for amygdala dysfunction

Philip Watson et al. Neuropsychol Rev. 2012 Sep.

Abstract

Systemic lupus erythematosus (SLE) is a multi-system autoimmune disorder characterized by the production of autoantibodies. Approximately 30-50 % of patients produce autoantibodies directed against N-Methyl-D-aspartic acid receptors (NMDARs). Once they have gained access to brain tissue, these autoantibodies bind to the NR2A subunit of the NMDARs and synergize with glutamate to cause excitatory, non-inflammatory cell death or alter neuron function. Both humans with SLE and animal models of SLE have shown structural and functional damage to the amygdala. The amygdala is a brain region important for processing the emotional relevance of stimuli in the environment. It also serves to modulate perception, attention, and memory to facilitate the processing and learning of relevant stimuli. Research has linked amygdala damage to deficits in emotional memory and emotional behavior. Individuals with SLE often exhibit emotional dysregulation, such as lability and depression; however, the behavioral impact of possible amygdala dysfunction has yet to be studied in this population. The purpose of this review is to 1) examine possible associations between SLE, anti-NMDAR antibodies, amygdala damage, and emotional processing deficits and 2) to identify the clinical, social, and treatment implications for individuals with SLE who suffer from deficits in emotional processing.

PubMed Disclaimer

Similar articles

Cited by

References

    1. Eur Neurol. 1999 Jul;42(1):41-8 - PubMed
    1. Behav Neurosci. 1994 Oct;108(5):1005-9 - PubMed
    1. Cogn Affect Behav Neurosci. 2002 Mar;2(1):52-63 - PubMed
    1. Biol Psychiatry. 2005 Feb 1;57(3):201-9 - PubMed
    1. Nat Med. 2001 Nov;7(11):1189-93 - PubMed

Publication types

MeSH terms

Substances

LinkOut - more resources