Depression in later life is associated with a high prevalence of cognitive impairments, which persist despite recovery, and structural brain changes on neuroimaging, including white matter lesions and atrophy. Depression has emerged as a risk factor for dementia and is now clearly established as a risk factor for the future development of vascular disease. The relationships between these features are not well understood, but it has been suggested that changes which occur during depression, such as hypercortisolaemia or immune activation, may be implicated. Raised cortisol levels, for example, are known to be associated with hippocampal damage in animals and in Cushing’s syndrome are associated with both hippocampal atrophy on MRI and cognitive impairments. The current study tested the hypothesis that biological changes during depression, particularly hypercortisoaemia, were aetiologically related to brain atrophy and persisting cognitive impairments. Elderly (age >60) subjects with DSM-IV major depression (n=43) and age-matched controls (n=40) underwent a 1.0 Tesla volumetric MRI scan, cognitive testing and salivary cortisol measurement. Depressed subjects showed deficits in multiple cognitive domains compared to controls, including impairments in attention, verbal and non-verbal memory, spatial working memory and executive function. They also exhibited significant hypercortisolaemia (mean AUC: depressed = 144.2nmol/l ±66.8; controls = 95.8nmol/l ±28.4, p<.001). However, there were no significant correlations between cognitive test measures and cortisol levels. Structural brain changes (hippocampal atrophy, frontal atrophy) were present only in those with late-onset depression and were related to persisting cognitive impairments. Results do not support the hypothesis that being depressed itself causes brain changes but instead suggests neurobiological changes as important aetiological factors in late-life depression.
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