Cerebrovascular changes and glucocorticoid mediated hippocampal atrophy
are considered relevant for depression-related cognitive deficits,
forming putative treatment targets.
This study examined the relative contribution of cortisol levels, brain
atrophy and white matter hyperintensities to the persistence of cognitive
deficits in older adults with depression.
Thirty-five people aged ⩾60 years with DSM–IV major depression and
twenty-nine healthy comparison controls underwent magnetic resonance
imaging (MRI) and were underwent magnetic resonance imaging (MRI) and
were followed up for 18 months. We analysed the relationship between
baseline salivary cortisol levels, whole brain, frontal lobe and
hippocampal volumes, severity of white matter hyperintensities and
follow-up cognitive function in both groups by testing the interaction
between the groups and these biological measures on tests of memory,
executive functions and processing speed in linear regression models.
Group differences in memory and executive function follow-up scores were
associated with ratings of white matter hyperintensities, especially of
the deep white matter and periventricular regions. Compared with healthy
controls, participants with depression scoring within the third tertile
of white matter hyperintensities dropped two and three standard
deviations in executive function and memory scores respectively. No
biological measure related to group differences in processing speed, and
there were no significant interactions between group and cortisol levels,
or volumetric MRI measures.
White matter hyperintensities, rather than cortisol levels or brain
atrophy, are associated with continuing cognitive impairments in older
adults with depression. The findings suggest that cerebrovascular disease
rather than glucocorticoid-mediated brain damage are responsible for the
persistence of cognitive deficits associated with depression in older