Neural evidence of disrupted self-referential processing in suicidal depression

Suicide remains a leading cause of death, particularly among young adults, highlighting the critical need to elucidate neural mechanisms underlying suicidality. This study used an event-related potential (ERP) paradigm to test whether depressed individuals with and without suicidal ideation show neural markers of altered semantic processing and conflict monitoring when reading clinically relevant self-referential content. During electroencephalography recording, depressed participants with (n=46) and without (n=44) suicidal ideation, and healthy controls (n=48), read first-person sentences whose final word rendered them congruent or incongruent with depression, suicidality, or neutral biographical experiences. Linear mixed-effects models were used to assess group and topic congruency effects on the N400 (semantic processing) and P600 (conflict monitoring/reanalysis). For neutral biographical (vs. non-biographical) sentences, all groups showed the expected reduction in N400 amplitudes, while the suicidal group exhibited significantly reduced P600 responses compared to the other groups. For depressive (vs. non-depressive) sentences, both depressed groups showed significantly reduced N400 amplitudes relative to controls and larger P600 amplitudes. For suicidal (vs. non-suicidal) sentences, there were no group differences in N400 amplitudes, but the suicidal group showed significantly attenuated P600 responses compared to controls. These results suggest that depressed individuals, regardless of suicidality, demonstrate facilitated semantic processing and increased reanalysis of depressive self-referential content, consistent with a negative self-schema. In contrast, those with suicidal ideation show reduced reanalysis of both neutral and suicidal self-referential content, possibly reflecting cognitive disengagement from personally relevant information. These patterns may support the potential utility of ERP markers for identifying individuals at elevated risk.