Phosphoinositide Signal Transduction Pathway and Major Depression

Mood disorders, including major depression (MD), overall constitute a major medical need. In fact, mood disorders require chronic treatments, lathough not effective in all patients. Multiple deficits, including cell atrophy and loss, were described in limbic and cortical brain regions of patients affected with mood disorders and in experimental animal models. A number of changes in gene expression and activity was described in brains of mood disorder affected patients. Therapies act reciprocally regulating many of these changes. Antidepressant and mood stabilizing therapies restore these deficits by reestablishing proper patterns of gene expression and function. Different signal transduction pathways play a role in the pathogenesis of mood disorders, namely the cyclic‐AMP, phosphoinositides (PI), mitogen‐activated protein kinase, and glycogen synthase kinase cascades. Although significant progresses have been achieved in studying the signal transduction pathways possibly involved in mood disorders, their reciprocal interconnection and the effect of alterations in human brain, many issues remain to be addressed. Knowledge of these intriguing aspects might help to clarify the pathogenesis of MD, widening the panel of available therapeutic tools.