Late-onset minor and major depression: early evidence for common neuroanatomical substrates detected by using MRI

Abstract

The purpose of our study was to examine the neuroanatomical correlates of late-onset minor and major depression and to compare them with similar measures obtained from nondepressed controls. Our study groups were comprised of 18 patients with late-onset minor depression, 35 patients diagnosed with late-onset major depression, and 30 nondepressed controls. All subjects were scanned by using a 1.5-tesla MRI scanner. Absolute whole brain volume and normalized measures of prefrontal and temporal lobe volumes were obtained and used for comparison among groups. Our findings indicate that patients with minor depression present with specific neuroanatomical abnormalities that are comparable with the major depression group but significantly different from the controls. Normalized prefrontal lobe volumes show a significant linear trend with severity of depression, with volumes decreasing with illness severity. Whole brain volumes did not differ significantly among groups. These findings have broad implications for the biology of late-life depression and suggest that there may be common neurobiological substrates that underlie all clinically significant forms of late-onset mood disturbances.

Temporal Lobe Atrophy and White Matter Lesions are Related to Major Depression over 5 years in the Elderly

“…Our findings suggest that structural neuropathological changes in the temporal lobes and WMLs are related to more severe depression rather than to the milder forms. This is supported by cross-sectional studies suggesting that temporal lobe atrophy (Kumar et al, 1998;Shah et al, 1998) may be related to severity of depression rather than to depression per se. However, minor depression was related to frontal lobe atrophy in the study by Kumar et al (1998).…”

“…This is supported by cross-sectional studies suggesting that temporal lobe atrophy (Kumar et al, 1998;Shah et al, 1998) may be related to severity of depression rather than to depression per se. However, minor depression was related to frontal lobe atrophy in the study by Kumar et al (1998). Differences may be explained by differences between population-based and clinical studies, cross-sectional and longitudinal studies, and the use of somewhat different diagnostic criteria.…”

“…Differences may be explained by differences between population-based and clinical studies, cross-sectional and longitudinal studies, and the use of somewhat different diagnostic criteria. We diagnosed minor depression based on DSM-IV criteria (n ¼ 58) or ICD codes (n ¼ 5), while Kumar et al (1998) diagnosed only according to DSM-IV, with the additional requirement that the symptoms should be present for at least 1 month. Thus, they may have looked at a more severe form of the disease compared with our study.…”

Mapping Callosal Morphology in Early- and Late-Onset Elderly Depression: An Index of Distinct Changes in Cortical Connectivity

“…Thinning of the callosal genu may also relate to decreased connectivity in prefrontal areas. Indeed, frontal lobe atrophy has been reported in late-onset depression (Almeida et al, 2002;Kumar et al, 1998). In addition, an attenuation of the 'normal' volumetric asymmetry in the frontal lobes was found in late-onset depressed subjects compared to healthy controls (Kumar et al, 2000).…”

“…Several distinctions between these groups have been identified, and subjects with early-onset depression are more likely to have a family history of psychiatric illness (Brodaty et al, 2001), while subjects with late-onset depression have greater subcortical ischemic disease (Krishnan et al, 1988;Salloway et al, 1996;Taylor et al, 2004). In addition, late-onset depression has been associated with more pronounced temporal lobe atrophy (Greenwald et al, 1997;Kumar et al, 1998) and hippocampal volume reductions (Steffens et al, 2000;Hickie et al, 2005), with specific genotypes possibly mediating this effect (Taylor et al, 2005). If these previous investigations are interpreted to be signs of different causes or risk factors for depression based on age at onset, greater splenium thinning in late-than early-onset depression might indeed point to more prominent atrophic or neurodegenerative processes in temporal connections, possibly reflecting higher risk for cognitive impairment and dementia conversion in the future (Geda et al, 2006;Salloway et al, 1996;Schweitzer et al, 2002;van Ojen et al, 1995).…”