Young Allan H, Juruena Mario F
Centre for Affective Disorders, Department of Psychological Medicine, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
Curr Top Behav Neurosci. 2021;48:1-20. doi: 10.1007/7854_2020_179.
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.
双相情感障碍病情严重且患病率高；尽管如此，其神经生物学机制仍远未阐明，这限制了新治疗方法的开发。虽然双相情感障碍的病因尚未完全明确，但人们认为该疾病可能是由导致易感性的遗传因素与诱发、促发和持续存在的环境因素（如压力和创伤性事件）之间的相互作用引起的。该疾病的病理生理机制表明，细胞内生化级联反应功能障碍、氧化应激和线粒体功能障碍会损害与神经元可塑性相关的过程，导致细胞损伤以及随后在尸检和神经影像学研究中发现的脑组织损失。我们所综述的数据表明，与激素、炎症、氧化应激和神经营养因子相关的外周生物标志物在双相情感障碍中会发生改变，尤其是在急性情绪发作期间。这些变化共同与该疾病的全身毒性以及多次发作所导致的损害有关。双相情感障碍中与复发发作相关的全身毒性可能会影响与双相情感障碍中压力进展和神经可塑性以及治疗反应相关的脑解剖学变化。
