In contrast to traditional perspectives of resilience as a stable, trait-like characteristic, resilience is now recognized as a multidimentional, dynamic capacity influenced by life-long interactions between internal and environmental resources. We review psychosocial and neurobiological factors associated with resilience to late-life depression (LLD). Recent research has identified both psychosocial characteristics associated with elevated LLD risk (e.g., insecure attachment, neuroticism) and psychosocial processes that may be useful intervention targets (e.g., self-efficacy, sense of purpose, coping behaviors, social support). Psychobiological factors include a variety of endocrine, genetic, inflammatory, metabolic, neural, and cardiovascular processes that bidirectionally interact to affect risk for LLD onset and course of illness. Several resilience-enhancing intervention modalities show promise for the prevention and treatment of LLD, including cognitive/psychological or mind–body (positive psychology; psychotherapy; heart rate variability biofeedback; meditation), movement-based (aerobic exercise; yoga; tai chi), and biological approaches (pharmacotherapy, electroconvulsive therapy). Additional research is needed to further elucidate psychosocial and biological factors that affect risk and course of LLD. In addition, research to identify psychobiological factors predicting differential treatment response to various interventions will be essential to the development of more individualized and effective approaches to the prevention and treatment of LLD.

The degree to which changes in caregiver burden over a one year period can be predicted by functioning of dementia patients and caregiver psychological stress was examined. The Direct Assessment of Functional Status (DAFS) was administered to 44 patients and the Caregiver Burden Inventory and the Brief Symptom Inventory were administered to their next-of-kin caregivers. All patients and caregivers were assessed at baseline and again in approximately one year with the same measures. Hierarchical regression revealed that baseline patient functioning predicted overall changes in caregiver burden, but that increases in psychological symptoms of caregivers such as depression, anxiety and hostility were the best predictors for specific types of increased caregiver burden, such as social, developmental, or physical burden. These results suggest that interventions should target reduction of particular psychological symptoms in order to reduce caregiver burden over time.

Previous research has identified patterns of cognitive deficits in patients with Alzheimer disease (AD), but little is known about their pattern of daily functional impairment. A total of 49 patients with AD and 52 healthy elderly controls were administered neuropsychological tests as well as the Direct Assessment of Functional Status (DAFS) test, an observation-based test of activities of daily living (ADLs). In this project, we assessed 14 separate tasks assessed by the DAFS. To analyze the data, 4 cognitive domains were created using neuropsychological composite z scores (means and standard deviation obtained from control data) for patients with AD. Results revealed that patients with AD performed worse on the memory, language, and visual-spatial relative to the executive domain. Additionally, patients with AD performed poorer than the controls on nearly all 14 DAFS tasks, with their worse performance being on the shopping-related tasks which, in part, requires memory skills. Logistic regression revealed better specificity than sensitivity classifications based on the DAFS tasks, and stepwise regression analyses indicated that cognitive domains predicted specific aspects of functional abilities. These findings suggest that patients with AD display a distinct pattern of ADLs performance, that traditional neuropsychological tests are useful in predicting daily functioning, and the DAFS has some strengths and weaknesses in classifying AD and controls.

The findings imply that increased apathy mediates the relationship between cognition and depression. The identification of mediating effects may inform future treatment strategies and preventive interventions that can focus on decreasing apathy to improve cognition in late-life depression.

Objective: Cognitive impairment is frequently comorbid with late-life depression (LLD) and often persists despite remission of mood symptoms with antidepressant treatment. Increasing understanding of factors that predict improvement of cognitive symptoms in LLD is useful to inform treatment recommendations. Methods: We used data from 2 randomized clinical trials of geriatric depression to examine the relationships between sociodemographic factors (resilience, quality of life) and clinical factors (age of depression onset, severity of depression, apathy) with subsequent cognitive outcomes. One hundred sixty-five older adults with major depression who had completed one of 2 clinical trials were included: (1) methylphenidate plus placebo, citalopram plus placebo, and citalopram plus methylphenidate or (2) citalopram combined with Tai Chi or health education. A comprehensive neuropsychiatric battery was administered; 2 measures of cognitive improvement were examined, one defined as an increase in general cognitive performance score of at least 1 standard deviation and the other 0.5 standard deviation pre–post treatment. Results: At posttreatment, 59% of participants had remitted, but less than a third of those who remitted showed cognitive improvement (29%). Cognitive improvement was observed in 18% of nonremitters. Lower baseline depression severity, greater social functioning, and depression onset prior to 60 years of age were significantly associated with cognitive improvement. None of the other measures, including baseline apathy, resilience, and depression remission status, were significantly associated with cognitive improvement. Conclusions: Lower severity of depression, earlier onset, and greater social functioning may predict improvement in cognitive functioning with treatment for depression in LLD.