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Article Abstract

Late-onset depression has been conceptualized as a neurologic disease. This view has been supportedby studies suggesting that late-onset depression is associated with cognitive impairment andneurologic 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 ledto the depression-executive dysfunction (DED) syndrome hypothesis. Subsequent studies suggestedthat DED has slow, poor, or abnormal response to classical antidepressants. DED is characterized bypsychomotor retardation, reduced interest in activities, impaired insight and pronounced behavioraldisability. This clinical presentation begs the question whether agents that can selectively activate internalvigilance and therefore improve alertness have beneficial effects on DED. There is early evidencethat psychosocial interventions aimed at improving the behavioral deficits of DED patients mayalso be effective in increasing remission rates and reducing depressive symptoms and disability.