Müller Walter E, Müller Juliane K
Med Monatsschr Pharm. 2016 Sep;39(9):371-6.
Bipolar disorders are quite common (lifetime prevalence 1–2 %) and have a substantial genetic risk (total heritability about 80 %). However, the contribution of individual genes to the total genetic risk is very small. Accordingly, no specific genes are known which show a larger contribution. Nevertheless, many of the known genes involved encode for proteins important for neural plasticity, mitochondrial function, dopaminergic neurotransmission and calcium channels. Similarly, the few data about neurobiological alterations in the brains of bipolar patients also point into the same direction. However, these observations are not very specific. A possible exception might be mitochondrial dysfunction seen in bipolar patients, which could integrate several of the other findings into one concept. The pharmacology of the drugs used to treat bipolar disorders is also not pointing to one common mechanism of action. While the mechanisms of action of antidepressants and antipsychotics probably are not different from the mechanisms relevant to treat depression and schizophrenia, the mechanisms of the anticonvulsants used in bipolar disorders (valproic acid, carbamazepine, lamotrigine) are probably different from their mechanism of action as anticonvulsant drugs. More likely, these drugs improve neuronal plasticity similarly to lithium and antidepressants.
双相情感障碍相当常见（终生患病率为1%-2%），且具有较高的遗传风险（总遗传度约为80%）。然而，单个基因对总遗传风险的贡献非常小。因此，目前尚不清楚有哪些特定基因具有更大的贡献。尽管如此，许多已知相关基因编码的蛋白质对神经可塑性、线粒体功能、多巴胺能神经传递和钙通道很重要。同样，关于双相情感障碍患者大脑神经生物学改变的少量数据也指向同一方向。然而，这些观察结果并非非常具有特异性。一个可能的例外是双相情感障碍患者中出现的线粒体功能障碍，它可能将其他一些发现整合到一个概念中。用于治疗双相情感障碍的药物药理学也未指向一种共同的作用机制。虽然抗抑郁药和抗精神病药的作用机制可能与治疗抑郁症和精神分裂症的相关机制并无不同，但双相情感障碍中使用的抗惊厥药（丙戊酸、卡马西平、拉莫三嗪）的作用机制可能与其作为抗惊厥药物的作用机制不同。更有可能的是，这些药物与锂盐和抗抑郁药类似，可改善神经元可塑性。
