Bipolar disorders are severe and have a high prevalence; despite this, the neurobiological mechanisms are far from being elucidated, and this limits the development of new treatments. Although the aetiology of bipolar disorders is not yet fully understood, it is accepted that the disorder(s) may result from the interaction between genetic factors that cause susceptibility and predisposing, precipitating and perpetuating environmental factors, such as stress and traumatic events. A pathophysiological formulation of the disease suggests that dysfunctions in intracellular biochemical cascades, oxidative stress and mitochondrial dysfunction impair the processes linked to neuronal plasticity, leading to cell damage and the consequent loss of brain tissue that has been identified in post-mortem and neuroimaging studies. The data we have reviewed suggests that peripheral biomarkers related to hormones, inflammation, oxidative stress and neurotrophins are altered in bipolar disorders, especially during acute mood episodes. Together, these changes have been associated with a systemic toxicity of the disease and the damage resulting from multiple episodes. Systemic toxicity related to recurrent episodes in bipolar disorder may influence brain anatomical changes associated with the progression of stress and neuroplasticity in bipolar disorder and the response to treatment.
Keywords: Bipolar disorder; Hormones; Inflammation; Neurobiology; Neuroendocrine; Neurotrophins; Oxidadtive stress.