Abstract
Many lupus patients develop neuropsychiatric manifestations, including cognitive dysfunction, depression, and anxiety. However, it is not clear if neuropsychiatric lupus is a primary disease manifestation, or is secondary to non-CNS disease. We found that MRL/lpr lupus-prone mice exhibited significant depression-like behavior already at 8 weeks of age, despite normal visual working memory, locomotor coordination and social preference. Moreover, depression was significantly correlated with titers of autoantibodies against DNA, NMDA receptors and cardiolipin. Our results indicate that lupus mice develop depression and CNS dysfunction very early in the course of disease, in the absence of substantial pathology involving other target organs.
MeSH terms
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Animals
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Aspartic Acid / analogs & derivatives
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Aspartic Acid / metabolism
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Autoantibodies / blood
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Brain / metabolism
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Brain / physiopathology
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Cardiolipins / immunology
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Choline / metabolism
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Chromatin / immunology
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Creatine / metabolism
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DNA / immunology
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Depression / etiology*
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Depression / immunology
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Depression / pathology
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Exploratory Behavior / physiology
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Female
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Lupus Erythematosus, Systemic / complications*
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Lupus Erythematosus, Systemic / immunology
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Lupus Erythematosus, Systemic / pathology
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Magnetic Resonance Imaging
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Magnetic Resonance Spectroscopy / methods
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Maze Learning / physiology
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Mice
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Mice, Mutant Strains
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Proteinuria / metabolism
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Psychomotor Performance / physiology
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Receptors, N-Methyl-D-Aspartate / immunology
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Recognition, Psychology / physiology
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Social Behavior
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Swimming
Substances
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Autoantibodies
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Cardiolipins
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Chromatin
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Receptors, N-Methyl-D-Aspartate
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Aspartic Acid
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DNA
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N-acetylaspartate
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Creatine
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Choline