The Effect of Aging in Inhibitory Control of Major Depressive Disorder Revealed by Event-Related Potentials

Abstract

Elderly depressed patients manifest pronounced executive dysfunction compared with younger subjects with depressive disorder. Aging-related brain changes may result in executive dysfunction in geriatric depression. We investigated the neural correlates of inhibitory control processing in depressed subjects at different ages using event-related potentials (ERPs). A equiprobable visual Go/Nogo task was used in 19 young (27.4 ± 5.0 years) and 18 elderly (70.8 ± 6.9 years) depressed subjects and their age-matched healthy controls (20 young subjects, 26.2 ± 3.7 years, and 18 elderly subjects, 68.1 ± 4.8 years). The responses were based on two types of equilateral triangular figures of upright (Go) and inverted triangle (Nogo). The elderly subjects exhibited later N2 and P3 latencies, and larger Go-N2 and P3 amplitudes, compared with the younger subjects. Further, the elderly controls displayed smaller P3 in the central and parietal regions, and yielded larger Nogo-P3 amplitude in the frontal region compared with younger controls. While the young depressed patients yielded smaller P3 amplitude than the controls across frontal, central and parietal regions, elderly depressed patients yielded smaller P3 than the elderly controls only in the frontal region. Our results suggest that the inhibitory control subprocesses are differentially affected by depression and aging. The stimulus response speed and the effort intensity of inhibition control are specifically impaired in the elderly depressed patients. And the diminished amplitudes of frontal P3 in the elderly depression imply a frontal dysfunction mechanism.

The Relationship Between Response-Inhibitory Event-Related Potentials and Symptoms of Attention-Deficit/Hyperactivity Disorder in Adult Patients with Major Depressive Disorder

“…This finding was observed whether or not it was adjusted for age, sex and education as covariates. Although there has been no previous study that evaluated Nogo N2 and P3 in patients with MDD comorbid with ADHD, our results are comparable to the previous studies showing decreased Nogo P3 amplitude in MDD subjects compared to normal patients [ 30 - 32 ]. The previous study showed a significant negative correlation between depressive symptoms and Nogo P3 amplitudes [ 32 ].…”

“…No previous Nogo N2 study of MDD with ADHD subjects has been reported. No study has reported significant changes in N2 latency in patient with MDD alone [ 30 , 31 ]. Moreover, few studies have reported changes in N2 latency among ADHD patients using the GoNogo paradigm, and no consistent findings have been reported [ 36 , 42 ].…”

“…In the Nogo condition, the N200 and the P300 were investigated at the Fz, FCz, and Cz electrodes. We focused on the changes of N2 and P3 at the frontocentral electrode, because MDD and ADHD have been regarded as mental illnesses associated with frontal-lobe dysfunction, and previous studies of MDD or ADHD patients generally showed changes of N2 and P3 in the fronto-central regions [ 30 , 31 , 34 , 39 , 47 ]. The time window we assumed was based on previous studies [ 48 ].…”

“…The changes in Nogo N2 and P3 amplitudes have been investigated to compare the disease characteristics of inattention and poor impulse control in both MDD and ADHD; however, the results have been inconsistent. Many studies of MDD have reported increased Nogo N2 or decreased P3 amplitude in MDD patients compared to healthy control [ 30 - 33 ]. However, some studies showed no difference in Nogo N2 or P3 amplitude [ 30 , 31 , 33 ].…”

“…Many studies of MDD have reported increased Nogo N2 or decreased P3 amplitude in MDD patients compared to healthy control [ 30 - 33 ]. However, some studies showed no difference in Nogo N2 or P3 amplitude [ 30 , 31 , 33 ]. ADHD patients were generally found to show decreased P3 amplitude [ 34 - 38 ].…”