Gray Matter Changes in Late Life Depression—a Structural MRI Analysis

Andreescu, Carmen; Butters, Meryl A.; Begley, Amy; Rajji, Tarek K.; Wu, Minxian; Meltzer, Carolyn C.; Reynolds, Charles F.; Aizenstein, Howard J.

doi:10.1038/sj.npp.1301655

Cited by 127 publications

(132 citation statements)

References 41 publications

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“…The majority of previous studies evaluating cortical volume loss in LLD have reported isolated regions of atrophy in LLD cortex (5–9), which in aggregate support extended neural network models of LLD, however integrating this data across studies is difficult due to methodological differences. Our findings of distributed reduction in cortical thickness in LLD is therefore significant and also largely consistent with the one previous study which has documented more distributed cortical volume loss in LLD (10). However, the degree to which our findings were almost exclusively seen in the right hemisphere was unanticipated and further study is warranted to determine if these findings are due in part to increased sensitivity of measures of cortical thickness over volumetric approaches to identifying cortical alterations in LLD.…”

Section: Discussionsupporting

confidence: 92%

“…However, the degree to which our findings were almost exclusively seen in the right hemisphere was unanticipated and further study is warranted to determine if these findings are due in part to increased sensitivity of measures of cortical thickness over volumetric approaches to identifying cortical alterations in LLD. In the previous study indicating a distributed pattern of cortical volume loss in LLD (10) laterality was not explored, so a direct comparison with our results is not possible. Nonetheless, our findings suggest that distributed reductions in cortical thickness may be a central morphometric abnormality associated with LLD and that cortical thinning in the right hemisphere may be particularly implicated.…”

Section: Discussionmentioning

confidence: 61%

“…While the etiology of late life depression (LLD) can be a complex interaction of psychological, medical, disability, and psychosocial factors (3, 4), LLD has also been consistently associated with cortical atrophy in bilateral frontal brain regions, most commonly in the orbitofrontal cortex (5–9), and to a lesser extent in parietal and temporal regions (10, 11). These findings largely support neurobiological conceptualizations of depression as being heavily mediated by extended neural networks comprised of the orbitofrontal cortex, the medial prefrontal cortex, the cingulate, and anatomical connections with the temporal lobe, striatum, thalamus and brain stem (12).…”

Section: Introductionmentioning

confidence: 99%

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Patterns of Reduced Cortical Thickness in Late-Life Depression and Relationship to Psychotherapeutic Response

Mackin

Tosun

Mueller

et al. 2013

The American Journal of Geriatric Psychiatry

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Objective Cortical atrophy has been associated with late life depression (LLD) and recent findings suggest that reduced right hemisphere cortical thickness is associated with familial risk for major depressive disorder but cortical thickness abnormalities in LLD have not been explored. Further, cortical atrophy has been posited as a contributor to poor antidepressant treatment response in LLD but the impact of cortical thickness on psychotherapy response is unknown. This study was conducted to evaluate patterns of cortical thickness in LLD and in relation to psychotherapy treatment outcomes. Methods Participants included 22 individuals with LLD and 12 age matched comparison subjects. LLD participants completed 12 weeks of psychotherapy and treatment response was defined as a 50% reduction in depressive symptoms. All participants participated in Magnetic Resonance Imaging (MRI) of the brain and cortical mapping of grey matter tissue thickness was calculated. Results LLD individuals demonstrated thinner cortex than controls prominently in the right frontal, parietal, and temporal brain regions. Eleven participants (50%) exhibited positive psychotherapy response after 12 weeks of treatment. Psychotherapy non-responders demonstrated thinner cortex in bilateral posterior cingulate and parahippocampal cortices, left paracentral, precuneus, cuneus, and insular cortices, and the right medial orbito-frontal and lateral occipital cortices relative to treatment responders. Conclusions Our findings suggest more distributed right hemisphere cortical abnormalities in LLD than have been previously reported. Additionally, our findings suggest that reduced bilateral cortical thickness may be an important phenotypic marker of individuals at higher risk for poor response to psychotherapy.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 61%

Section: Introductionmentioning

confidence: 99%

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Patterns of Reduced Cortical Thickness in Late-Life Depression and Relationship to Psychotherapeutic Response

Mackin

Tosun

Mueller

et al. 2013

The American Journal of Geriatric Psychiatry

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“…9,10 Finally, researchers have reported that the putamen is activated most strongly during anticipation of reward, whereas the caudate is activated most strongly during the receipt of reward. 8,10,11 A growing body of research indicates that adults with MDD have smaller volumes of the caudate [12][13][14][15] and putamen 13,14,16,17 than healthy controls. Postmortem studies have also reported smaller putamen volumes in depressed than in nondepressed adults.…”

Section: Introductionmentioning

confidence: 99%

Accelerated aging of the putamen in patients with major depressive disorder

Sacchet

Camacho

Livermore

et al. 2017

JPN

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IntroductionMajor depressive disorder (MDD) is primarily characterized by depressed mood and a blunted experience of pleasure (i.e., anhedonia). 1 The disorder is prevalent and chronic and represents a substantial personal, social and economic burden. [2][3][4] Neuroscience promises to elucidate mechanisms under lying depressive pathophysiology, leading to more effective approaches to the prevention and treatment of this debilitating disorder.Considerable evidence indicates that reward processing is dysfunctional in individuals with MDD. 5,6 The basal ganglia (BG) are a set of subcortical structures, including the striatum (caudate and putamen), nucleus accumbens and pallidum, that are critically involved in these reward processing steps. 7Previously research has indicated that depressed individuals have decreased activation in the striatum, 5,6 and some investigators have hypothesized that this abnormal activity affects decision-making. 5 Research in both animals and humans suggests that the dorsal striatum is involved in action selection and initiation and in encoding and integrating sensorimotor, cognitive and motivational/emotional information.8 Current evidence is mixed regarding specific roles of the putamen and caudate in reward processing. The results of several studies using fMRI suggest that whereas the putamen specifi cally encodes reward-related feedback, the caudate encodes both reward and punishment feedback.9,10 Finally, researchers have reported that the putamen is activated most strongly during anticipation of reward, whereas the caudate is activated most strongly during the receipt of reward. 8,10,11 A growing body of research indicates that adults with MDD have smaller volumes of the caudate 12-15 and putamen 13,14,16,17 than healthy controls. Postmortem studies have also reported smaller putamen volumes in depressed than in nondepressed adults. 18 It is important to note that these studies typically include adult samples with a mean age older than 40 years. Depression-associated differences in BG volumes are less consistent in samples of both younger adults 19,20 and adolescents. 21 It appears, therefore, that this discrepancy is associated with age differences in the study Background: Growing evidence indicates that major depressive disorder (MDD) is characterized by accelerated biological aging, including greater age-related changes in physiological functioning. The disorder is also associated with abnormal neural reward circuitry, particularly in the basal ganglia (BG). Here we assessed age-related changes in BG volume in both patients with MDD and healthy control participants. Methods: We obtained whole-brain T 1 -weighted images from patients with MDD and healthy controls. We estimated grey matter volumes of the BG, including the nucleus accumbens, caudate, pallidum and putamen. Volumes were assessed using multivariate analysis of covariance (MANCOVA) with age as a covariate, followed by appropriate post hoc tests. Results: We included 232 individuals (116 patients with MDD) in our analy...

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“…Both methods involve spatial normalization of the brain images to a standard stereotactic space by registration to an atlas image. Automated ROI methods (or brain parcellation) are frequently used to study structural brain anomalies in schizophrenia patients (Lopez-Garcia et al, 2006;Yamasue et al, 2004) and recently are gaining popularity in aging research to demonstrate non-linear relationships between brain volumes and age (Andreescu et al, 2007;Terribilli et al, in press). …”

Section: Introductionmentioning

confidence: 99%

Voxel-based morphometry and automated lobar volumetry: The trade-off between spatial scale and statistical correction

Voormolen¹,

Wei²,

Chow³

et al. 2010

NeuroImage

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Voxel-based morphometry (VBM) and automated lobar region of interest (ROI) volumetry are comprehensive and fast methods to detect differences in overall brain anatomy on magnetic resonance images. However, VBM and automated lobar ROI volumetry have detected dissimilar gray matter differences within identical image sets in our own experience and in previous reports. To gain more insight into how diverging results arise and to attempt to establish whether one method is superior to the other, we investigated how differences in spatial scale and in the need to statistically correct for multiple spatial comparisons influence the relative sensitivity of either technique to group differences in gray matter volumes. We assessed the performance of both techniques on a small dataset containing simulated gray matter deficits and additionally on a dataset of 22q11-deletion syndrome patients with schizophrenia (22q11DS-SZ) vs. matched controls. VBM was more sensitive to simulated focal deficits compared to automated ROI volumetry, and could detect global cortical deficits equally well. Moreover, theoretical calculations of VBM and ROI detection sensitivities to focal deficits showed that at increasing ROI size, ROI volumetry suffers more from loss in sensitivity than VBM. Furthermore, VBM and automated ROI found corresponding GM deficits in 22q11DS-SZ patients, except in the parietal lobe. Here, automated lobar ROI volumetry found a significant deficit only after a smaller subregion of interest was employed. Thus, sensitivity to focal differences is impaired relatively more by averaging over larger volumes in automated ROI methods than by the correction for multiple comparisons in VBM. These findings indicate that VBM is to be preferred over automated lobarscale ROI volumetry for assessing gray matter volume differences between groups.

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Gray Matter Changes in Late Life Depression—a Structural MRI Analysis

Cited by 127 publications

References 41 publications

Patterns of Reduced Cortical Thickness in Late-Life Depression and Relationship to Psychotherapeutic Response

Patterns of Reduced Cortical Thickness in Late-Life Depression and Relationship to Psychotherapeutic Response

Accelerated aging of the putamen in patients with major depressive disorder

Voxel-based morphometry and automated lobar volumetry: The trade-off between spatial scale and statistical correction

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