A Prospective Study of Depression and Immune Dysregulation in Multiple Sclerosis

Mood Disorders and Dysfunction of the Hypothalamic-Pituitary-Adrenal Axis in Multiple Sclerosis

“…Such a causal relation between mood disorders and brain pathology would also be in accordance with the higher rate of depression in MS compared with other severely disabling diseases, 37,38 the frequent occurrence of depression in patients with MS even before the onset of neurologic symptoms, 39 and the interesting correlation between affective disorders and the CD4/CD8 ratio or CD8 + cell counts, as presumed indicators of chronic immunoactivation. 27 In contrast, the lack of correlation between affective symptoms and extent of disability observed in this study is not consistent with earlier interpretations that mood disorders merely represent emotional reactions to disability. 1,26 This clinical study, however, does not demonstrate such causal relationships or exclude the role of numerous other factors, eg, psychosocial variables or personality, in the pathogenesis of mood disorders and HPA dysfunction.…”

Mood Disorders and Dysfunction of the Hypothalamic-Pituitary-Adrenal Axis in Multiple Sclerosis

“…Such a causal relation between mood disorders and brain pathology would also be in accordance with the higher rate of depression in MS compared with other severely disabling diseases, 37,38 the frequent occurrence of depression in patients with MS even before the onset of neurologic symptoms, 39 and the interesting correlation between affective disorders and the CD4/CD8 ratio or CD8 + cell counts, as presumed indicators of chronic immunoactivation. 27 In contrast, the lack of correlation between affective symptoms and extent of disability observed in this study is not consistent with earlier interpretations that mood disorders merely represent emotional reactions to disability. 1,26 This clinical study, however, does not demonstrate such causal relationships or exclude the role of numerous other factors, eg, psychosocial variables or personality, in the pathogenesis of mood disorders and HPA dysfunction.…”

Treatment of Depression Is Associated With Suppression of Nonspecific and Antigen-Specific TH1 Responses in Multiple Sclerosis

“…However, the effect sizes were robust, and the statistical methods employed controlled for the effects of chance based on sample size. Furthermore, our findings are consistent with those of previous cross-sectional 17,24 and longitudinal 18,25 studies. 2We considered placebo treatment of major depressive disorder unethical.…”

“…54 In the absence of a placebo control condition, it is possible that all patients showed unusually high autoimmune reactivity before treatment and that the observed changes reflect the natural course of such reactivity independent of treatment for depression. This interpretation, while not consistent with the existing literature, 13,14,18,24,25,39,42,55 cannot be ruled out. (3) Because this study was of short duration, we do not know if observed changes in IFN-␥ production are of clinical significance.…”

Depressive symptoms, anxiety and cognitive impairment: emerging evidence in multiple sclerosis

“…Conversely, the harmful role of proinflammatory cytokines is consistent among different studies [ 40 , 41 ]. Pro-inflammatory cytokines may affect serotonin synthesis and reuptake in the CNS, and, consequently, may lead to the malfunctioning of noradrenergic and serotoninergic circuits that represent the pathways targeted by several antidepressant drugs [ 42 – 44 ].…”

Mood Disorders and Dysfunction of the Hypothalamic-Pituitary-Adrenal Axis in Multiple Sclerosis

“…Such a causal relation between mood disorders and brain pathology would also be in accordance with the higher rate of depression in MS compared with other severely disabling diseases, 37,38 the frequent occurrence of depression in patients with MS even before the onset of neurologic symptoms, 39 and the interesting correlation between affective disorders and the CD4/CD8 ratio or CD8 + cell counts, as presumed indicators of chronic immunoactivation. 27 In contrast, the lack of correlation between affective symptoms and extent of disability observed in this study is not consistent with earlier interpretations that mood disorders merely represent emotional reactions to disability. 1,26 This clinical study, however, does not demonstrate such causal relationships or exclude the role of numerous other factors, eg, psychosocial variables or personality, in the pathogenesis of mood disorders and HPA dysfunction.…”

Treatment of Depression Is Associated With Suppression of Nonspecific and Antigen-Specific TH1 Responses in Multiple Sclerosis

“…However, the effect sizes were robust, and the statistical methods employed controlled for the effects of chance based on sample size. Furthermore, our findings are consistent with those of previous cross-sectional 17,24 and longitudinal 18,25 studies. 2We considered placebo treatment of major depressive disorder unethical.…”

“…54 In the absence of a placebo control condition, it is possible that all patients showed unusually high autoimmune reactivity before treatment and that the observed changes reflect the natural course of such reactivity independent of treatment for depression. This interpretation, while not consistent with the existing literature, 13,14,18,24,25,39,42,55 cannot be ruled out. (3) Because this study was of short duration, we do not know if observed changes in IFN-␥ production are of clinical significance.…”

Depressive symptoms, anxiety and cognitive impairment: emerging evidence in multiple sclerosis

“…Conversely, the harmful role of proinflammatory cytokines is consistent among different studies [ 40 , 41 ]. Pro-inflammatory cytokines may affect serotonin synthesis and reuptake in the CNS, and, consequently, may lead to the malfunctioning of noradrenergic and serotoninergic circuits that represent the pathways targeted by several antidepressant drugs [ 42 – 44 ].…”

Mood Disorders and Dysfunction of the Hypothalamic-Pituitary-Adrenal Axis in Multiple Sclerosis

“…Such a causal relation between mood disorders and brain pathology would also be in accordance with the higher rate of depression in MS compared with other severely disabling diseases, 37,38 the frequent occurrence of depression in patients with MS even before the onset of neurologic symptoms, 39 and the interesting correlation between affective disorders and the CD4/CD8 ratio or CD8 + cell counts, as presumed indicators of chronic immunoactivation. 27 In contrast, the lack of correlation between affective symptoms and extent of disability observed in this study is not consistent with earlier interpretations that mood disorders merely represent emotional reactions to disability. 1,26 This clinical study, however, does not demonstrate such causal relationships or exclude the role of numerous other factors, eg, psychosocial variables or personality, in the pathogenesis of mood disorders and HPA dysfunction.…”

Treatment of Depression Is Associated With Suppression of Nonspecific and Antigen-Specific TH1 Responses in Multiple Sclerosis

“…However, the effect sizes were robust, and the statistical methods employed controlled for the effects of chance based on sample size. Furthermore, our findings are consistent with those of previous cross-sectional 17,24 and longitudinal 18,25 studies. 2We considered placebo treatment of major depressive disorder unethical.…”

“…54 In the absence of a placebo control condition, it is possible that all patients showed unusually high autoimmune reactivity before treatment and that the observed changes reflect the natural course of such reactivity independent of treatment for depression. This interpretation, while not consistent with the existing literature, 13,14,18,24,25,39,42,55 cannot be ruled out. (3) Because this study was of short duration, we do not know if observed changes in IFN-␥ production are of clinical significance.…”

Depressive symptoms, anxiety and cognitive impairment: emerging evidence in multiple sclerosis

“…Conversely, the harmful role of proinflammatory cytokines is consistent among different studies [ 40 , 41 ]. Pro-inflammatory cytokines may affect serotonin synthesis and reuptake in the CNS, and, consequently, may lead to the malfunctioning of noradrenergic and serotoninergic circuits that represent the pathways targeted by several antidepressant drugs [ 42 – 44 ].…”