Dissertations, Theses, and Capstone Projects

Date of Degree


Document Type


Degree Name





Joel Sneed

Committee Members

Faith Gunning

Laura Rabin

Subject Categories

Clinical Psychology | Mental Disorders | Other Psychiatry and Psychology | Other Psychology | Psychiatric and Mental Health | Psychological Phenomena and Processes


Apathy, late-life depression, salience network, reward network, incentive salience


Background and Significance: Apathy is a common comorbidity in late-life depression. Among older depressed adults, apathy is associated with a number of adverse outcomes, including increased disability, comorbid illness, and mortality. The etiological substrates of apathy in late-life depression nonetheless remain poorly understood, and little is known about its optimal treatment. To this end, the aim of the current study was to examine cortical abnormalities within the salience (SN) and reward networks (RN), two brain systems involved in the processing of incentive salience that may underlie the syndrome of apathy in older depressed adults.

Methods: We examined the association between apathy and cortical thickness of the right insula, caudal anterior cingulate cortex (cACC), rostral anterior cingulate cortex (rACC), medial orbitofrontal cortex (mOFC), and lateral orbitofrontal cortex (lOFC) in 49 individuals with late-life depression before and after 12 weeks of antidepressant treatment with the selective serotonin reuptake inhibitor (SSRI) escitalopram. Apathy was quantified using the Apathy Evaluation Scale (AES). Cortical thickness was computed using FreeSurfer. Regions of interest (ROIs) were parcellated using the Desikan-Killiany atlas.

Results: Within the SN, cortical thickness of the insula was significantly associated with response of apathy symptoms to escitalopram, as well as persistence of apathy symptoms after 12 weeks of treatment. Thickness of the cACC, which is involved in both salience and reward processing, was not associated with apathy at any time. Within the RN, thickness of the rACC was significantly related to apathy at baseline. Thickness of the mOFC and lOFC was not associated with apathy at any time. Exploratory analyses examining the association between cognitive functions and apathy revealed a relationship between response of apathy to treatment and several aspects of cognition, including processing speed, executive functioning (i.e., set shifting and source monitoring), and memory (i.e., retrieval of verbal information).

Conclusions: The results of this study suggest a role for abnormalities within both the SN and RN in older depressed adults with apathy. Given the interplay between structures of the SN and RN in processing of incentive salience, older depressed adults with apathy may have a decreased ability to associate an anticipated outcome with the experience of desire, thereby decreasing motivated, goal-directed activity.