Depression results from changes in the central nervous system (CNS) that may result from immunological abnormalities. The immune system affects the CNS through cytokines, which regulate brain activities and emotions. Cytokines affect two biological systems that are most associated with the pathophysiology of depression: The hypothalamic-pituitary-adrenal axis and the catecholamine/sympathetic nervous system. Neuroinflammation and cytokines affect the brain signal patterns involved in the psychopathology of depression and the mechanisms of antidepressants, and they are associated with neurogenesis and neural plasticity. These observations suggest that neuroinflammation and cytokines might cause and/or maintain depression, and that they might be useful in the diagnosis and prognosis of depression. This psychoneuroimmunologic perspective might compensate for some of the limitations of the monoamine theory by suggesting that depression is a result of a failure to adapt to stress and that inflammatory responses and cytokines are involved in this process. In this review, the interactions of cytokines with the CNS, neuroendocrine system, neurotransmitters, neurodegeneration/neurogenesis, and antidepressants are discussed. The roles of cytokines in the etiology and psychopathology of depression are examined. The use of cytokine inhibitors or anti-inflammatory drugs in depression treatment is explored. Finally, the significance and limitations of the cytokine hypothesis are discussed.

Neuroinflammation and cytokine abnormality in major depression: Cause or consequence in that illness?

The hypothalamic-pituitary-adrenal (HPA) axis and its end-effectors glucocorticoid hormones play central roles in the adaptive response to numerous stressors that can be either internal or external. Thus, this system has a strong impact on the brain hippocampus and its major functions, such as cognition, memory as well as behavior, and mood. The hippocampal area of the adult brain contains neural stem cells or more committed neural progenitor cells, which retain throughout the human life the ability of self-renewal and to differentiate into multiple neural cell lineages, such as neurons, astrocytes, and oligodendrocytes. Importantly, these characteristic cells contribute significantly to the above-indicated functions of the hippocampus, while various stressors and glucocorticoids influence proliferation, differentiation, and fate of these cells. This review offers an overview of the current understanding on the interactions between the HPA axis/glucocorticoid stress-responsive system and hippocampal neural progenitor cells by focusing on the actions of glucocorticoids. Also addressed is a further discussion on the implications of such interactions to the pathophysiology of mood disorders.

/pdf/stress-glucocorticoid-hormones-and-hippocampal-neural-1f4d7ee6f2.pdf

Stress, glucocorticoid hormones, and hippocampal neural progenitor cells: implications to mood disorders.

Ever since the time of the Roman physician Galen in 200 AD, evidence has been provided to indicate that bacterial and viral infections, autoimmune diseases, cancers as well as predisposition to heart disease frequently increase in patients with major depression [1]. Previously such phenomena were thought to be coincidental partly because there was a lack of a theoretical framework whereby such diverse phenomena could be associated with an abnormality in brain function which is presumed to cause depression. However, during the past 20 years, evidence has accumulated showing that profound changes occur in both cellular and non cellular immunity in patients with major depression and that such changes could be causally linked to the onset of physical ill health [2]. While the mechanisms linking these phenomena are complex, stress undoubtedly plays a key role in triggering many of the changes. It is known that corticotrophin releasing factor (CRF) is elevated in the cerebrospinal fluid of untreated depressed patients which is associated with the hypercortisolaemia that is a common feature of major depression [3]. The rise in cortisol causes a suppression of some aspects of cellular (e.g. natural killer cell, T-lymphocyte replication) immunity [15] which might contribute to the vulnerability of the patient to various infections. However, not all aspects of cellular immunity are suppressed in the depressed patient.

Brain cytokines and the psychopathology of depression

We studied 60 patients receiving a 1-year course of interferon (IFN)-αtherapy for chronic viral hepatitis. Patients underwent psychiatric assessment before starting the IFN-αtherapy, and monthly throughout the therapy, using the Structured Clinical Interview for the DSM-III-R, the 17-item Hamilton Depression Rating Scale, the Beck Depression Inventory and the Spielberg State and Trait Anxiety Inventory. Five patients had a baseline diagnosis of major depression and 18 (30%) developed an IFN-α-induced psychiatric adverse effect; 12 of these 23 patients received psychopharmacological treatment (patients and clinicians jointly decided the need for treatment). Two of the five patients with baseline depression started an antidepressant treatment (paroxetine) together with the IFN-α and successfully completed the IFN-αtherapy. Ten patients received treatment for the IFN-α-induced psychiatric adverse effects (depression in five patients, anxiety in two patients, severe irritability in two patients and insomnia i...

Psychopharmacological Treatment of Depression, Anxiety, Irritability and Insomnia in Patients Receiving Interferon-α: a Prospective Case Series and a Discussion of Biological Mechanisms

Depression, stress and immunological activation: the role of cytokines in depressive disorders.

P.1.155 Steroid-independent translocation of the glucocorticoid receptor by the antidepressant, desipramine

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P.1.155 Steroid-independent translocation of the glucocorticoid receptor by the antidepressant, desipramine