Inflammatory Monocytes in Bipolar Disorder and Related Endocrine Autoimmune Diseases

Bipolar disorder (also called manic-depressive illness) is one of the major mood disorders. The term manic-depressive illness was introduced by Emil Kraepelin (1856-1926) in the late nineteenth century.1 It is in most patients a chronic illness with recurrent manic and depressive episodes, usually alternated with periods with normal mood between the episodes. A manic episode is characterised by an elevated, expansive or irritable mood which can be accompanied by a high self-esteem, decreased need of sleep, flight of ideas or racing thoughts, increased speech, distractibility, psychomotor agitation and excessive involvement in activities with painful consequences. A hypomanic episode meets the criteria for mania but is not associated with social or occupational impairment as is the case with a manic episode. A patient with a depressed episode has a depressed mood together with the possible following symptoms: sleep disturbances, psychomotor retardation or agitation, fatigue, feelings of worthlessness or guilt, impaired thinking or concentration, change of appetite or weight and suicidal thoughts.2, 3 With its manic episodes bipolar disorder differs from (unipolar) depression, which is characterized by one or more depressive episodes, but never a manic (or hypomanic) episode

Recent advances in psychoneuroimmunology: inflammation in psychiatric disorders

Psychiatric disorders are common and complex and their precise biological underpinnings remain elusive. Multiple epidemiological, molecular, genetic and gene expression studies suggest that immune system dysfunction may contribute to the risk for developing psychiatric disorders including schizophrenia, bipolar disorder, and major depressive disorder. However, the precise mechanisms by which inflammation-related events confer such risk are unclear. In this review, we examine the peripheral and central evidence for inflammation in psychiatric disorders and the potential molecular mechanisms implicated including inhibition of neurogenesis, apoptosis, the HPA-axis, the role of brain-derived neurotrophic factor and the interplay between the glutamatergic, dopaminergic and serotonergic neurotransmitter systems