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Int. J. Mol. Sci. 2015, 16(5), 10281-10300; doi:10.3390/ijms160510281

Anti-NR2A/B Antibodies and Other Major Molecular Mechanisms in the Pathogenesis of Cognitive Dysfunction in Systemic Lupus Erythematosus

1,2,* and 1,2
1
Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, 21 Lower Kent Ridge Road, Singapore 119077, Singapore
2
Divison of Rheumatology, Department of Medicine, National University Hospital, National University Health System, 1E Kent Ridge Road, Singapore 119228, Singapore
*
Author to whom correspondence should be addressed.
Academic Editors: Chak-Sing Lau and Vera Sau-Fong Chan
Received: 23 March 2015 / Revised: 20 April 2015 / Accepted: 29 April 2015 / Published: 6 May 2015
View Full-Text   |   Download PDF [1188 KB, uploaded 6 May 2015]   |  

Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disease that affects approximately 1–45.3 per 100,000 people worldwide. Although deaths as a result of active and renal diseases have been substantially declining amongst SLE patients, disease involving the central nervous system (CNS), collectively termed neuropsychiatric systemic lupus erythematosus (NPSLE), remains one of the important causes of death in these patients. Cognitive dysfunction is one of the most common manifestations of NPSLE, which comprises deficits in information-processing speed, attention and executive function, in conjunction with preservation of speech. Albeit a prevalent manifestation of NPSLE, the pathogenetic mechanisms of cognitive dysfunction remain unclear. Recent advances in genetic studies, molecular techniques, neuropathology, neuroimaging and cognitive science have gleaned valuable insights into the pathophysiology of lupus-related cognitive dysfunction. In recent years, a role for autoantibodies, molecular and cellular mechanisms in cognitive dysfunction, has been emerging, challenging our previous concept of the brain as an immune privileged site. This review will focus on the potential pathogenic factors involved in NPSLE, including anti-N-methyl-d-aspartate receptor subunit NR2A/B (anti-NR2A/B) antibodies, matrix metalloproteinase-9, neutrophil extracellular traps and pro-inflammatory mediators. Better understanding of these mechanistic processes will enhance identification of new therapeutic modalities to halt the progression of cognitive decline in SLE patients. View Full-Text
Keywords: cognitive dysfunction; anti-NR2A/B antibodies; matrix metalloproteinase-9; neutrophil extracellular traps; pro-inflammatory mediators; systemic lupus erythematosus cognitive dysfunction; anti-NR2A/B antibodies; matrix metalloproteinase-9; neutrophil extracellular traps; pro-inflammatory mediators; systemic lupus erythematosus
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Tay, S.H.; Mak, A. Anti-NR2A/B Antibodies and Other Major Molecular Mechanisms in the Pathogenesis of Cognitive Dysfunction in Systemic Lupus Erythematosus. Int. J. Mol. Sci. 2015, 16, 10281-10300.

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