distal sources, in part due to lower signal-to-noise ratios in the measurement of frontal EEG activity than those derived from the CSD reference (Hagemann et al., 2001). In order for frontal EEG asymmetry to be an endophenotype for depression risk , it must converge with other possible risk indicators for depression (e.g., genetic variations in serotonin genes involved in the transmission and maintenance of depression), and CSD-referenced EEG asymmetry appears most promising in this endeavor.
