Abstract

Along with the increase in reported figures of depression in the world's population, organizations such as the WHO have begun to promote screening and pharmacological treatment of mild symptomatic cases. The problem in this context is that the manifestations of 'normal' and 'pathological' depressive mood do not differ much from each other, which creates difficulties at a diagnostic and scientific level. This article explores an approach that could facilitate the clinical and scientific task of differentiating between non-specific affective disturbances (depressive mood) and depression as an illness as such. It is proposed that various causal stressors interact with individual predispositions to trigger a transient change in mood as an adaptive response. In turn, the greater the intensity of the stressors (psychological, social, etc.), the greater the neuroinflammation, which would diminish neuronal plasticity and the possibilities of mood compensation and behavioral change of the subject. The existence of this neurobiological alteration (decreased neuronal plasticity), rather than depressive mood, would help us to categorize depression as a disease.

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