While much research has demonstrated a relationship between depression and cognitive deficits, most studies have neglected to include measurements of performance validity. The very small number of studies that have examined this relationship when accounting for performance validity have found that the relationship between depression and cognition is small or nonsignificant. The current study examined the relationship between depression (assessed through both clinical interview and self-report symptom measures) and multiple domains of cognition after accounting for noncredible performance on neuropsychological testing.

Participants were veterans referred for outpatient clinical evaluation. Among other tests that varied across patients, the neuropsychological battery included: California Verbal Learning Test - second edition (CVLT-II) total immediate recall across trials 1–5, short delay free recall, and long delay free recall; Trail Making Test; FAS and Animal Fluency; Rey–Osterrieth Complex Figure Test (ROCF) copy and 3-minute delay recall; and Wisconsin Card Sorting Test (WCST) categories completed, total errors, and percent perseverative errors. These tests represent domains that have previously been examined in relation to depression (e.g., memory, processing speed, executive functioning). Evaluations were conducted for clinical purposes, so that some individuals who were not administered certain tests have missing data. The first set of regression analyses (N=206) included age, sex, and education at Step 1, Beck Depression Inventory-2 (BDI-2) total score at Step 2, and pass or failure of Trial 1 of the Test of Memory Malingering (TOMM) at Step 3 as predictors of performance on the 12 test indices. The second set of regression analyses (N=559) mirrored the first but with Major Depressive Disorder (MDD) diagnosis at Step 2 instead.

In the first set of analyses, after including TOMM in the model, only the relationship between BDI-2 and verbal fluency remained significant, but did not survive Bonferroni correction (p<.004). In the second set of analyses, before including the TOMM, MDD diagnosis was significantly related only to worse performance on Trails A and CVLT-II Short and Long Delay Free Recall, with small effect sizes (rp=.06–.15). When TOMM Trial 1 was included in the model, MDD diagnosis became a nonsignificant predictor of CVLT-II Long Delay Free Recall but remained a significant predictor for Trails A and CVLT-II Short Delay Free Recall (p<.05). After Bonferroni correction (p<.004), with TOMM Trial 1 included in the model, MDD diagnosis remained a significant predictor only of CVLT-II Short Delay Free Recall, with a small effect size (rp=.17).

After accounting for noncredible performance, there was little evidence for a relationship between depression diagnosis or symptoms and many cognitive domains. These results suggest that previously reported effects of depression on cognition are not mainly due to underlying neurological mechanisms, but rather to motivational factors. Future research could focus on the potential psychological mechanisms (e.g., negative attitudes, expectancy bias, low motivation, etc.) driving the relationship between depression and low effort on cognitive testing. If replicated, the current findings could be valuable to clinicians treating depressed individuals who have concerns about their cognitive functioning, by indicating psychoeducation and reassurance.