Neuropsychiatric manifestations of depression in multiple sclerosis: Neuroinflammatory, neuroendocrine, and neurotrophic mechanisms in the pathogenesis of immune-mediated depression

Michele L Pucak, Katherine A L Carroll, Douglas A. Kerr, Adam I Kaplin

Research output: Contribution to journalArticle

Abstract

Evidence suggests that depression in multiple sclerosis (MS) is largely biologically mediated by some of the same processes involved in the immunopathogenesis of this neurologic disease. In particular, the increase in proinflammatory cytokines, activation of the hypothalamic-pituitary-adrenal (HPA) axis, and reduction in neurotrophic factors that occur in MS may each account for the increased rate of depression seen in MS. The possible contributions of these neuroinflammatory, neuroendocrine, and neurotrophic mechanisms suggest a diverse array of novel treatment strategies for depression, both in the context of inflammatory conditions as well as in idiopathic depression. Furthermore, if such processes in MS play a causative role in the pathogenesis of depression, and depression in turn has affects on neurophysiological processes related to immune function, then treatment of depression might have a positive effect on MS disease progression. This makes treating MS depression a neuropsychiatric imperative.

Original languageEnglish (US)
Pages (from-to)125-139
Number of pages15
JournalDialogues in Clinical Neuroscience
Volume9
Issue number2
StatePublished - 2007

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Multiple Sclerosis
Depression
Nerve Growth Factors
Nervous System Diseases
Disease Progression
Cytokines

Keywords

  • Cytokine
  • Hypothalamic-pituitary-adrenal axis
  • Inflammation
  • Interferon
  • Neuroimaging
  • Treatment

ASJC Scopus subject areas

  • Neuropsychology and Physiological Psychology
  • Neuroscience(all)

Cite this

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title = "Neuropsychiatric manifestations of depression in multiple sclerosis: Neuroinflammatory, neuroendocrine, and neurotrophic mechanisms in the pathogenesis of immune-mediated depression",
abstract = "Evidence suggests that depression in multiple sclerosis (MS) is largely biologically mediated by some of the same processes involved in the immunopathogenesis of this neurologic disease. In particular, the increase in proinflammatory cytokines, activation of the hypothalamic-pituitary-adrenal (HPA) axis, and reduction in neurotrophic factors that occur in MS may each account for the increased rate of depression seen in MS. The possible contributions of these neuroinflammatory, neuroendocrine, and neurotrophic mechanisms suggest a diverse array of novel treatment strategies for depression, both in the context of inflammatory conditions as well as in idiopathic depression. Furthermore, if such processes in MS play a causative role in the pathogenesis of depression, and depression in turn has affects on neurophysiological processes related to immune function, then treatment of depression might have a positive effect on MS disease progression. This makes treating MS depression a neuropsychiatric imperative.",
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AU - Kaplin, Adam I

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