The evolution in the understanding of the neurobiology of most prevalent mental disorders such as major depressive disorder (MDD), bipolar disorder or schizophrenia has not gone hand in hand with the synthesis and clinical use of new drugs that would represent a therapeutic revolution such as that brought about by selective serotonin reuptake inhibitors (SSRIs) or atypical antipsychotics. Although scientists are still a long way from understanding its true aetiology, the neurobiological concept of depression has evolved from receptor regulation disorder, to a neurodegenerative disorder with a hippocampal volume decrease with the controversial reduction in neurotrophins such as BDNF, to current hypotheses that consider depression to be an inflammatory and neuroprogressive process. As regards antidepressants, although researchers are still far from knowing their true mechanism of action, they have gone from monoaminergic hypotheses, in which serotonin was the main protagonist, to emphasising the anti-inflammatory action of some of these drugs, or the participation of p11 protein in their mechanism of action.In the same way, according to the inflammatory hypothesis of depression, it has been proposed that some NSAIDS such as aspirin or drugs like simvastatin that have an anti-inflammatory action could be useful in some depressive patients. Despite the fact that there may be some data to support their clinical use, common sense and the evidence advise us to use already tested protocols and wait for the future to undertake new therapeutic strategies.

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Three neurotransmitter systems are implicated in the biological basis of depression: the serotonergic system is thought to be a major component in the development of depression and in the efficacy of antidepressant drugs, while the noradrenergic and dopaminergic systems play lesser roles, but are important in the development of antidepressant side-effects. Selective serotonin re-uptake inhibitors (SSRIs) are still the drug treatments of choice in major depressive disorder, but each has a subtly different pharmacological profile, which has implications for pharmacodynamic actions and clinical efficacy and side-effect profiles. Although the precise mechanisms responsible for specific depressive symptoms are not yet well defined, evidence is emerging that some SSRIs may be more effective in combating certain symptoms than others. Fluoxetine appears to be particularly effective in overcoming symptoms of fatigue and low energy, whereas paroxetine or sertraline may be more appropriately used for depressed patients experiencing anxiety. A growing understanding of molecular mechanisms in depression and the unique clinical consequences of each pharmacological agent brings us one step closer to being able to individualize antidepressant treatment on the basis of core presenting symptoms and the needs of the individual patient. ( Int J Psych Clin Pract 2001; 5 (Suppl 1): S19-S28).

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