Neuropsychiatric systemic lupus erythematosus: Pathophysiology and the future of treatment

Takahisa Gono, Takeshi Takarada, Yasuhiro Katsumata, Yasushi Kawaguchi, Yukio Yoneda, Hisashi Yamanaka

Research output: Contribution to journalReview articlepeer-review


Systemic lupus erythematosus (SLE) is characterized by the presence of several autoantibodies, including anti-dsDNA. Among types of SLE, neuropsychiatric (NP)-SLE accounts for significant morbidity and mortality. Cerebrovascular disease, which could account for most of the serious permanent neurological damage, is a common presentation of NP-SLE. The pathophysiology of NP-SLE involves several factors, including vasculitis, thrombosis, and inflammation and/or apoptosis of neuronal and glial cells. The current treatment strategy is immunosuppressive therapy, which is occasionally insufficient for patients with NP-SLE. Recent studies have revealed that autoantibodies, such as anti-NR2, pass from the peripheral blood to the brain through the blood-brain barrier, cross-react with human brain tissue and cause increased intracellular Ca2+ in SLE. Regulating blood-brain barrier permeability, inhibiting autoantibody deposition in tissues and modulating intracellular Ca2+ may be new concepts for the treatment with NP-SLE.

Original languageEnglish
Pages (from-to)585-595
Number of pages11
JournalInternational Journal of Clinical Rheumatology
Issue number5
Publication statusPublished - Oct 1 2013
Externally publishedYes


  • anti-NR2
  • antiphospholipid
  • antiribosomal P
  • autoantibodies
  • blood-brain barrier permeability
  • cross-reactivity
  • intracellular Ca signaling
  • neuropsychiatric symptoms
  • systemic lupus erythematosus

ASJC Scopus subject areas

  • Rheumatology


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