ABSTRACT
A critical question regarding the etiopathogenesis of bipolar disorder is whether there is a cellular endophenotype that can explain abnormalities at the level of dysfunctional neurons and circuits. A recent study has suggested that apoptosis could play a role in the pathophysiology of bipolar disorder. Is it possible that this abnormality is related to an endophenotype for this disorder? Fundamental differences in the genetic regulation of the apoptotic cascade, electron transport chain, and antioxidation enzymes are present and uniquely different from those seen in schizophrenia. These differences may reflect the cellular endophenotype for bipolar disorder and are revieved below.
