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Association of Hippocampal Atrophy With Cerebrospinal Fluid Antibodies Against the NR2 Subtype of the N ‐Methyl‐ D ‐Aspartate Receptor in Patients With Systemic Lupus Erythematosus and Patients With Primary Sjögren's Syndrome
Author(s) -
Lauvsnes Maria B.,
Beyer Mona K.,
Kvaløy Jan Terje,
Greve Ole J.,
Appenzeller Simone,
Kvivik Ingeborg,
Harboe Erna,
Tjensvoll Anne B.,
Gøransson Lasse G.,
Omdal Roald
Publication year - 2014
Publication title -
arthritis and rheumatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.106
H-Index - 314
eISSN - 2326-5205
pISSN - 2326-5191
DOI - 10.1002/art.38852
Subject(s) - hippocampal formation , cerebrospinal fluid , atrophy , medicine , antibody , pathology , immunology
Objective Cognitive dysfunction is common in both systemic lupus erythematosus (SLE) and primary Sjögren's syndrome (SS). Antibodies against the NR2 subtype of the N ‐methyl‐ D ‐aspartate receptor (anti‐NR2 antibodies) cause hippocampal atrophy and cognitive impairment in mice and have been associated with memory impairment in both patients with SLE and patients with primary SS. In addition, a reduced volume of hippocampal gray matter has been demonstrated in both SLE and primary SS. This study was undertaken to investigate whether there is a connection between the presence of anti‐NR2 antibodies and hippocampal atrophy in human diseases. Methods Fifty patients with SLE and 50 patients with primary SS underwent clinical examination and cerebral magnetic resonance imaging. Anti‐NR2 antibodies in cerebrospinal fluid (CSF) were measured, and hippocampal gray matter volumes were compared between patients who were positive for and those who were negative for anti‐NR2 antibodies. Results Patients with anti‐NR2 antibodies in CSF had less hippocampal gray matter than patients without these antibodies. No other differences regarding gray matter volumes in other parts of the brain were identified. Conclusion The present findings indicate that anti‐NR2 antibodies in patients with SLE and primary SS cause neuronal death manifested as reduced hippocampal gray matter, as has been previously demonstrated in mice with autoimmune disease.