Abstract
Late life depression is a complex disease associated with a number of contributing neurobiological factors, including cerebrovascular disease, neurodegeneration, and inflammation, which also contribute to its longitudinal prognosis and course. These factors create a context in which the brain is more vulnerable to the impact of stress, and thus, to depression. At the same time, some individuals are protected from late life depression and its consequences, even in the face of neurobiological vulnerability, through benefitting from one or more attributes associated with resilience, including social support, engagement in physical and cognitive activities, and brain reserve. Enhanced understanding of how neurobiological and environmental factors interact in predicting vulnerability and resilience is needed to predict onset and course of depression in late life and develop more effective interventions.
Highlights
Late-life depression (LLD; defined as depression occurring in individuals age 65 or older, and distinct from late onset depression, which is a subtype of depression with onset after the age of 65) has been associated with high incidence of chronic illness, cognitive dysfunction, disability, and poor prognosis [1,2,3,4,5]
Frontal lobe volume and brain lesion volume were not correlated. Together these findings suggest that vascular and neurodegenerative processes may be autonomous pathways contributing to LLD, independent of one another in the context of LLD
Given structural imaging findings and results from epidemiological community studies suggesting an increased risk of Alzheimer’s disease (AD) among those with depression, there has been work investigating the presence of neuropathological features of neurodegenerative disease in post-mortem-brain tissue, these studies are limited in number and sample sizes are small
Summary
Late-life depression (LLD; defined as depression occurring in individuals age 65 or older, and distinct from late onset depression, which is a subtype of depression with onset after the age of 65) has been associated with high incidence of chronic illness, cognitive dysfunction, disability, and poor prognosis [1,2,3,4,5]. There is wide support for the suggestion that for at least a subset of individuals with LLD, vascular changes, including hypoperfusion of and disrupted connection between regions relevant to cognition and affective regulation are one mechanism of depression in late life and its associated symptoms.
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