Neuroanatomical substrates of depression in the elderly

Krishnan, K. Ranga Rama; McDonald, William M.; Doraiswamy, P. Murali; Tupler, Larry A.; Husain, Mustafa M.; Boyko, Orest B.; Figiel, Gary S.; Ellinwood, Everett H.

doi:10.1007/bf02191522

Cited by 171 publications

(93 citation statements)

References 14 publications

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“…We should note here that our results do not replicate previously reported differences in caudate volumes between [12][13][14][15] and it is possible that the observed group differences were qualified by an interaction with age. Other studies examined a different age group than we did, 13 and many had smaller samples (e.g., patient groups of fewer than 30 individuals).…”

Section: J Psychiatry Neurosci 2017;42(3)contrasting

confidence: 99%

“…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%

“…It is also worth noting that many of these studies have used small samples of participants (e.g., patient groups with fewer than 30 individuals). 13,18,20,[22][23][24][25] Recently the Enhancing NeuroImaging Genetics through Meta-Analysis (ENIGMA) MDD working group has addressed the issue of underpowered single studies by conducting large-scale meta-analyses of neuro imaging studies of MDD. In a recent meta-analysis from this group that included 1728 individuals with MDD and more than 7199 control participants across 15 samples, only hippocampal volumes differentiated MDD from control participants.…”

Section: Introductionmentioning

confidence: 99%

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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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Section: J Psychiatry Neurosci 2017;42(3)contrasting

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Accelerated aging of the putamen in patients with major depressive disorder

Sacchet

Camacho

Livermore

et al. 2017

JPN

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“…These data are consistent with findings of frontal lobe impairment in biochemical (10), anatomical (11) and histological (9) investigations in the brains of patient with a history of depressive disorders (3,12).…”

Section: Jrc Almeida Et Alsupporting

confidence: 91%

Late-life depression, heart failure and frontal white matter hyperintensity: a structural magnetic resonance imaging study

Almeida

Alves

Wajngarten

et al. 2005

Braz J Med Biol Res

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The relevance of the relationship between cardiac disease and depressive symptoms is well established. White matter hyperintensity, a bright signal area in the brain on T2-weighted magnetic resonance imaging scans, has been separately associated with cardiovascular risk factors, cardiac disease and late-life depression. However, no study has directly investigated the association between heart failure, major depressive symptoms and the presence of hyperintensities. Using a visual assessment scale, we have investigated the frequency and severity of white matter hyperintensities identified by magnetic resonance imaging in eight patients with late-life depression and heart failure, ten patients with heart failure without depression, and fourteen healthy elderly volunteers. Since the frontal lobe has been the proposed site for the preferential location of white matter hyperintensities in patients with late-life depression, we focused our investigation specifically on this brain region. Although there were no significant group differences in white matter hyperintensities in the frontal region, a significant direct correlation emerged between the severity of frontal periventricular white matter hyperintensity and scores on the Hamilton scale for depression in the group with heart failure and depression (P = 0.016, controlled for the confounding influence of age). There were no significant findings in any other areas of the brain. This pattern of results adds support to a relationship between cardiovascular risk factors and depressive symptoms, and provides preliminary evidence that the presence of white matter hyperintensities specifically in frontal regions may contribute to the severity of depressive symptoms in cardiac disease. Correspondence

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“…28 One way vascular disease might lead an individual to develop LLD is by causing brain lesions that directly disrupt the neural network underlying mood and thus the capacity to regulate mood, and subsequently depressive symptoms. Though data supporting a causal link between vascular disease and LLD is difficult to obtain and thus lacking, correlative data supporting the vascular depression hypothesis include MRI studies of the brain of individuals with LLD showing increased rates of white-matter hyperintensities compared to non-depressed age-matched controls 32-33 and the finding that these white-matter hyperintensities correlate with functional changes in the mood neural network. 34 …”

Section: Current Hypotheses For Biological Mechanisms Promoting Lldmentioning

confidence: 99%

The Age-by-Disease Interaction Hypothesis of Late-Life Depression

McKinney

Sibille

2013

The American Journal of Geriatric Psychiatry

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The phenomenological diagnosis of depression is successful in increasing diagnostic reliability, but it is a classification scheme without biological bases. One subtype of depression for which evidence suggests a unique biological basis is late-life depression (LLD), with first onset of symptoms after the age of 65. LLD is common and poses a significant burden on affected individuals, caretakers, and society. The pathophysiology of LLD includes disruptions of the neural network underlying mood, which can be conceptualized as the result of dysfunction in multiple underlying biological processes. Here, we briefly review current LLD hypotheses and then describe the characteristics of molecular brain aging and their overlap with disease processes. Further, we propose a new hypothesis for LLD, the Age-by-Disease Interaction hypothesis, which posits that the clinical presentation of LLD is the integrated output of specific biological processes that are pushed in LLD-promoting directions by changes in gene expression naturally occurring during brain aging, hence leading the brain to a physiological state that is more susceptible to LLD, since additional pushes by genetic, environmental and biochemical factors may now be sufficient to generate dysfunctional states that produce depressive symptoms. We put our propositions together into a decanalization model to aid in illustrating how age-related biological changes of the brain can shift the repertoire of available functional states in a pro-depression direction, and how additional factors can readily lead the system into distinct and stable maladaptive phenotypes, including LLD. This model brings together basic research on neuropsychiatric and neurodegenerative diseases more closely with the investigation of normal aging. Specifically, identifying biological processes affected during normal aging may inform the development of new interventions for the prevention and treatment of LLD.

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Neuroanatomical substrates of depression in the elderly

Cited by 171 publications

References 14 publications

Accelerated aging of the putamen in patients with major depressive disorder

Accelerated aging of the putamen in patients with major depressive disorder

Late-life depression, heart failure and frontal white matter hyperintensity: a structural magnetic resonance imaging study

The Age-by-Disease Interaction Hypothesis of Late-Life Depression

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