Symposia
Health Psychology / Behavioral Medicine - Adult
Naoise Mac Giollabhui, M.A.
Massachusetts General Hospital
SOMERVILLE, Massachusetts
Lauren Ellman, Ph.D.
Professor
Temple University
Philadelphia, Pennsylvania
Marin Kautz, M.A.
Graduate Student in Clinical Psychology
Temple University
Philadelphia, Pennsylvania
Tania Giovannetti, Ph.D.
Professor
Temple University
Philadelphia, Pennsylvania
Lauren B. Alloy, Ph.D.
Temple University
Philadelphia, Pennsylvania
Background: A substantial subset of depressed individuals exhibit deficits in cognitive functioning that persist when depression is in remission. It remains unclear why only certain persons exhibit these deficits, what the underlying mechanism is, and which cognitive domains are affected. Theory and substantial empirical evidence suggest that chronic inflammation may underlie persistent cognitive dysfunction in remitted depression, as a subset of depressed individuals exhibit a pro-inflammatory phenotype and chronic inflammation has been directly linked with cognitive dysfunction in clinically depressed persons and medical, elderly, and healthy adult samples. This study tested how youth with a history of depression and chronic inflammation exhibited worse cognitive functioning in three specific domains.
Method: Individuals (n = 80) who were tracked over 8 years participated in a follow-up assessment during which global cognitive functioning (IQ), executive functioning (EF), episodic memory, and psychomotor speed were assessed. All participants had completed repeated assessments of immune biomarkers, depressive symptoms, and EF as part of the parent study. Chronic inflammation was defined as individuals repeatedly exhibiting elevated C reactive protein (using a clinical cutoff: 3mg/L) at >50% of assessments and depression history was defined as Children’s Depression Inventory score≥19.
Results: In cross-sectional analyses, individuals with a history of depression and chronic inflammation performed worse on an index of EF (b=-.33, p< .05; based on 7 measures) and episodic memory (b=-.29, p< .05; based on 3 measures) but not psychomotor speed; analyses controlled for current depressive symptoms, IQ, socioeconomic status, and age. In prospective analyses of the two measures of EF that were repeatedly assessed, individuals with chronic inflammation and depression combined performed worse on all three subsets of the digit span (working memory; p’s< .05), but not on a measure of switching attention. Notably, overall performance on the working memory tasks declined over time for individuals with a combination of chronic inflammation and depression history (β=-1.48, p< .05).
Conclusion: Adolescents who have experienced depression and who exhibit a pro-inflammatory phenotype experience persistent difficulties in EF and episodic memory. Moreover, this study suggests that the combination of depression and chronic inflammation during this developmental period may be associated with a decline in working memory.