Systemic lupus erythomatosus (SLE), often simply called lupus, is a complex autoimmune disease marked by joint pain, skin rashes, extreme fatigue, and depression, among other symptoms. Some studies have described a possible link between SLEs most severe psychiatric manifestation, psychosis, and a protein autoantibody associated with the central nervous system, anti-ribosomal P.
To investigate how an autoantibody could stimulate behavioral changes by interaction with the brain, researchers at Tel Aviv University set out to induce depressive hallmarks in mice. Their findings, presented in the March 2007 issue of Arthritis & Rheumatism (http://www.interscience.wiley.com/journal/arthritis), shed light on the brain pathways of depression in general and in central nervous system dysfunction in SLE in particular.
Healthy female mice received injections, directly into the brain, of human anti-ribosomal P antibodies extracted from the blood sample of an SLE patient. For control purposes, equal numbers of mice were injected with normal human immunoglobin G. All the mice were then subjected to a series of tests: a forced swimming test in a glass beaker partially filled water to evaluate escape-oriented behaviors, such as rearing and jumping; rotarod and grip strength tests to gauge motor function; a staircase test; a swim T-maze test to assess cognitive function; and a passive avoidance test to measure the ability of mice to remember a foot shock delivered 24-hours earlier.
Depression-like behavior was strongly observed in the performance of anti-ribosomal P antibody-injected mice on the forced swimming test. The immobility time of these mice was twice as high as that of the control group, indicating a state of despair. In the remaining tests of cognitive and motor functions, there were no significant differences detected between the mice in each group, ruling out neurol
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