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Review
. 2007;9(2):125-39.
doi: 10.31887/DCNS.2007.9.2/mpucak.

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

Michele L Pucak  1 , Katherine A L Carroll, Douglas A Kerr, Adam I Kaplin
Affiliations
Review

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

Michele L Pucak et al. Dialogues Clin Neurosci. 2007.

Abstract
in English, Spanish, French

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.

La evidencia sugiere que la depresión en la esclerosis múltiple (EM) está mediada en gran medida biológicamente por algunos de los mismos procesos involucrados en la inmunopatogénesis de esta enfermedad neurológica. En especial, el aumento de citoquinas proinflamatorias, la activación del eje HHA y la reducción de los factores neurotróficos que ocurre en la EM pueden dar cuenta del aumento de la frecuencia de depresión observada en la EM. La posible contribución de estos mecanismos neuroinflamatorio, neuroendocrino y neurotrófico sugieren una serie diferente de nuevas estrategias de tratamiento para la depresión, tanto en el contexto de condiciones inflamatorias como en la depresión idiopática. Además, si tales procesos en la EM tienen un rol causal en la patogénesis de la depresión, y la depresión a su vez tiene efectos en los procesos neurofisiológicos relacionados con la función inmune, entonces el tratamiento de la depresión es posible que tenga un efecto positivo en la progresión de la EM. De esto se deduce que el tratamiento de la depresión en la EM es un imperativo neuropsiquiátrico.

Certains processus impliqués dans l'immunopatho-genèse de la sclérose en plaques (SEP) semblent intervenir en grande partie biologiquement dans la dépression qui lui est associée. En particulier, l'augmentation des cytokines pro-inflammatoires, l'activation de l'axe HPA et la réduction des facteurs neurotrophiques au cours de la SEP entrent en jeu dans l'augmentation des taux de dépression observés dans cette pathologie. Les implications éventuelles de ces mécanismes neuro-inflammatoires, neuroendocriniens et neurotrophiques laissent entrevoir la possibilité d'un large éventail de nouvelles stratégies thérapeutiques pour la dépression, aussi bien dans le contexte des pathologies inflammatoires que dans celui de la dépression idiopathique. Si de plus ces processus liés à la SEP sont responsables de la pathogenèse de la dépression, et que celle-ci influe à son tour sur les processus neuropsychologiques liés à la fonction immunitaire, le traitement de la dépression pourrait alors avoir un effet positif sur la progression de la SEP Le traitement de la dépression liée à la SEP devient donc un impératif neuropsychiatrique.

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