Basic data for bipolar disorders: genetics, neurobiology and pharmacology.

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.