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Article Abstract

Late-onset depression has been conceptualized as a neurologic disease. This view has been supported by studies suggesting that late-onset depression is associated with cognitive impairment and neurologic comorbidity that may or may not be clinically evident when depression is first diagnosed. Findings implicating a dysfunction of frontostriatal-limbic pathways in geriatric depression have led to the depression-executive dysfunction (DED) syndrome hypothesis. Subsequent studies suggested that DED has slow, poor, or abnormal response to classical antidepressants. DED is characterized by psychomotor retardation, reduced interest in activities, impaired insight and pronounced behavioral disability. This clinical presentation begs the question whether agents that can selectively activate internal vigilance and therefore improve alertness have beneficial effects on DED. There is early evidence that psychosocial interventions aimed at improving the behavioral deficits of DED patients may also be effective in increasing remission rates and reducing depressive symptoms and disability.