Additionally, there is a growing appreciation that new medications that simply imitate “traditional” drugs, those aiming to directly or indirectly alter monoaminergic throughput,

may be of limited benefit to those patients with refractory depression. Those strategies assume that the target circuits are functionally intact and that changes in synaptic activity will alter the postsynaptic throughput of the system. The evidence discussed here indicates that, in addition to neurochemical changes, many patients suffering from mood disorders also have marked structural alterations in crucial neuronal circuits. Therefore, in order to obtain an optimal treatment response, it Inhibitors,research,lifescience,medical will most likely be crucial to provide both trophic and neurochemical support. The aim of the trophic support would be to enhance and maintain normal synaptic connectivity, therefore permitting the chemical Inhibitors,research,lifescience,medical signal to restore maximum functioning of vital circuits essential for normal affective functioning.

In fact, preliminary studies suggest that regional structural changes in the brains of patients with mood disorders may be related with Inhibitors,research,lifescience,medical not only severity and duration of the illness, but also with altered treatment response to pharmacotherapy and ECT. The evidence also suggests that, somewhat similar Inhibitors,research,lifescience,medical to the treatment of other chronic medical

conditions, such as hypertension and diabetes, prompt and sustained treatment may be necessary to prevent many of the injurious learn more long-term sequelae associated with mood disorders. Although the evidence hints at an association between hippocampal atrophy and illness duration in depressed patients, it remains unclear Inhibitors,research,lifescience,medical whether the volumetric and cellular changes observed in other brain areas are related to affective episodes. In fact, some studies have described reduced gray matter volumes and increased ventricle size in patients with mood disorders at the time of their first episode and in early onset of the disease.12,15 In conclusion, relevant genotypes for mood disorders are being identified, and clinical research techniques are now capable of defining neurobiological phenotypes. below Similarly, results from transcriptomic and proteomic studies which identified neurotrophic signaling as targets for the long-term actions of antidepressants and mood stabilizers have played a role (along with neuroimaging and postmortem brain studies) in a reconceptualization about the pathophysiology, course, and optimal long-term treatment of severe mood disorders. These data suggest that, while mood disorders are clearly not classical neurodegenerative diseases, they are in fact associated with impairments of cellular plasticity and resilience.