All Publications


  • Androgen treatment effects on hippocampus structure in boys with Klinefelter syndrome. Psychoneuroendocrinology Foland-Ross, L. C., Ross, J. L., Reiss, A. L. 2018; 100: 223–28

    Abstract

    Klinefelter syndrome (KS, 47,XXY) is the most common sex chromosome aneuploidy in males. A variety of complex clinical needs is associated with KS, including physical, cognitive and psychosocial impairments. Standard treatment for KS consists of androgen replacement therapy in adolescence to offset testosterone deficiency. Such treatment has a beneficial effect on the physical and behavioral manifestations of this syndrome. Whether androgen supplementation has a significant influence on the brain, however, is unknown. In the current study, we examined regional gray matter volume in boys with KS to assess whether treatment with oxandrolone, a synthetic hormone analog of testosterone, was associated with structural changes in the brain. Specifically, we focused our investigation on the hippocampus, given (1) its involvement in KS, and (2) the high concentration of androgen receptors found in this region. Structural magnetic resonance imaging data was acquired from a subsample of boys who completed a 2-year double-blind clinical trial in which patients were randomized to treatment with oxandrolone or to placebo, as well as from a sample of typically developing (TD) boys. Group differences in hippocampal volume were examined. A significant main effect of group was observed. Pairwise comparisons indicated smaller hippocampal volume in the placebo group relative to the oxandrolone group, as well as smaller volume in the placebo group relative to the TD control group. No difference in volume was observed between the treatment and TD groups. Moreover, across KS subgroups, a significant positive association was observed between hippocampus volume and performance on a spatial memory task, indicating treatment-based changes in brain structure may underlie cognitive change. These findings confirm prior reports implicating a role of the hippocampus in KS and are important in extending previous research by demonstrating a significant effect of androgens on brain structure.

    View details for PubMedID 30388596

  • Neural correlates of liraglutide effects in persons at risk for Alzheimer's Disease. Behavioural brain research Watson, K. T., Wroolie, T. E., Tong, G., Foland-Ross, L. C., Frangou, S., Singh, M., McIntyre, R., Roat-Shumway, S., Myoraku, A., Reiss, A. L., Rasgon, N. L. 2018

    Abstract

    Insulin resistance (IR) is a metabolic state preceding development of type 2 diabetes (DM2), cardiovascular disease, and neurodegenerative disorders, including Alzheimer's Disease (AD). Liraglutide, a glucagon-like peptide-1 (GLP) agonist, is an insulin-sensitizing agent with neuroprotective properties, as shown in animal studies. The purpose of this double-blinded, placebo-controlled study was to examine the neural effects of administration of liraglutide in cognitively normal late middle-aged individuals with subjective cognitive complaints (half of subjects had family history of AD). Seed-based resting state connectivity using functional magnetic resonance imaging (fMRI) conducted before and after 12 weeks of liraglutide treatment or placebo. Neuropsychological testing was conducted before and after treatment to determine whether there were any potential behavioral correlates to neural changes.RESULTS: At baseline (time point 1), higher fasting plasma glucose (FPG) was associated with decreased connectivity between bilateral hippocampal and anterior medial frontal structures. At time point 2, we observed significant improvement in intrinsic connectivity within the default mode network (DMN) in the active group relative to placebo. There were no detectable cognitive differences between study groups after this duration of treatment. To our knowledge, this is the first placebo-controlled study to report neural effects of liraglutide in a middle-aged population with subjective cognitive complaints. Larger and longer duration studies are warranted to determine whether liraglutide has neuroprotective benefit for individuals at risk for AD.

    View details for PubMedID 30099030

  • Neural correlates of top-down regulation and generation of negative affect in major depressive disorder PSYCHIATRY RESEARCH-NEUROIMAGING Davis, E., Foland-Ross, L. C., Gotlib, I. H. 2018; 276: 1–8

    Abstract

    Major depressive disorder (MDD) is characterized by biased information processing that leads to difficulties regulating negative affect, which includes difficulty decreasing negative affect as well as maladaptively increasing negative affect via cognitive processes. To examine the underlying neural correlates, we scanned depressed and never-depressed adults as they completed a cognitive reappraisal task which required decreasing negative affect while viewing a negative image (down-regulation) and increasing negative affect while viewing a neutral image (emotion generation). Compared to control participants, MDD participants had less recruitment of the dorsal anterior cingulate (dACC) and supplementary motor area (SMA) during early phases of down-regulation, the latter associated with poorer negative affect regulation. Further, MDD participants exhibited greater recruitment of the right middle temporal gyrus (MTG) during emotion generation, which was associated with lower negative affect. Dysregulated negative affect in MDD may be due to impairments in efficiently activating the dACC and SMA to meet regulation demands, and maladaptive generation of negative affect that characterizes individuals with MDD may be counteracted by compensatory activation in the MTG. Elucidating neural mechanisms that underlie the generation of negative affect in the absence of external stimuli is an important extension of previous work examining dysfunctional emotional processes in MDD.

    View details for PubMedID 29689500

  • Longitudinal assessment of hippocampus structure in children with type 1 diabetes. Pediatric diabetes Foland-Ross, L. C., Reiss, A. L., Mazaika, P. K., Mauras, N., Weinzimer, S. A., Aye, T., Tansey, M. J., White, N. H., Diabetes Research in Children Network (DirecNet) 2018

    Abstract

    The extant literature finds that children with type 1 diabetes mellitus (T1D) experience mild cognitive alterations compared to healthy age-matched controls. The neural basis of these cognitive differences is unclear but may relate in part to the effects of dysglycemia on the developing brain. We investigated longitudinal changes in hippocampus volume in young children with early-onset T1D. Structural magnetic resonance imaging data were acquired from 142 children with T1D and 65 age-matched control subjects (4-10years of age at study entry) at 2 time points, 18 months apart. The effects of diabetes and glycemic exposure on hippocampal volume and growth were examined. Results indicated that although longitudinal hippocampus growth did not differ between children with T1D and healthy control children, slower growth of the hippocampus was associated with both increased exposure to hyperglycemia (interval HbA1c) and greater glycemic variability (MAGE) in T1D. These observations indicate that the current practice of tolerating some hyperglycemia to minimize the risk of hypoglycemia in young children with T1D may not be optimal for the developing brain. Efforts that continue to assess the factors influencing neural and cognitive development in children with T1D will be critical in minimizing the deleterious effects of diabetes.

    View details for PubMedID 29675980

  • Like Mother Like Daughter: Putamen Activation as a Mechanism Underlying Intergenerational Risk for Depression. Social cognitive and affective neuroscience Colich, N. L., Ho, T. C., Ellwood-Lowe, M., Foland-Ross, L. C., Sacchet, M. D., LeMoult, J. L., Gotlib, I. H. 2017

    Abstract

    Having a depressed mother is one of the strongest predictors for developing depression in adolescence. Given the role of aberrant reward processing in the onset and maintenance of depression, we examined the association between mothers' and their daughters' neural response to the anticipation of reward and loss. Fifteen non-depressed mothers with a history of recurrent depression and their never-disordered daughters, and 23 mothers without past or current depression and their never-disordered daughters, underwent fMRI while performing the monetary incentive delay (MID) task. To assess mother-daughter concordance, we first identified ROIs involved in the anticipation of reward and loss across all mother-daughter pairs. Within each of these ROIs, we examined the association between mothers' and daughters' neural response, and the interaction between group status and mothers' neural response in predicting daughters' neural response. We found a significant association between mothers' and daughters' putamen response to the anticipation of loss, regardless of mother's depression history. Furthermore, pubertal stage moderated the association between mother-daughter putamen concordance. Our findings suggest a unique role of the putamen in the maternal transmission of reward learning and have important implications for understanding disorders characterized by disturbances in reward learning and processing, such as major depression.

    View details for DOI 10.1093/scan/nsx073

    View details for PubMedID 28575505

  • Hyperactivation in cognitive control and visual attention brain regions during emotional interference in adolescent depression Biological Psychiatry: Cognitive Neuroscience and Neuroimaging Colich, N., Ho, T., Foland-Ross, L., Eggleston, C., Ordaz, S., Singh, M., Gotlib, I. 2017
  • Relationships Between Altered Functional Magnetic Resonance Imaging Activation and Cortical Thickness in Patients With Euthymic Bipolar I Disorder. Biological psychiatry : cognitive neuroscience and neuroimaging Joshi, S. H., Vizueta, N., Foland-Ross, L., Townsend, J. D., Bookheimer, S. Y., Thompson, P. M., Narr, K. L., Altshuler, L. L. 2016; 1 (6): 507-517

    Abstract

    Performance during cognitive control functional magnetic resonance imaging (fMRI) tasks are associated with frontal lobe hypoactivation in patients with bipolar disorder, even while euthymic. Here, we study the structural underpinnings for this functional abnormality simultaneously with brain activation data.In a sample of ninety adults (45 with inter-episode Bipolar I disorder and 45 healthy controls), we explored whether abnormal functional activation patterns in bipolar euthymic subjects during a Go-NoGo fMRI task are associated with regional deficits in cortical gray matter thickness in the same regions. Cross-sectional differences in fMRI activation were used to form a-priori hypotheses for region-of-interest cortical gray matter thickness analyses. fMRI BOLD to structural magnetic resonance imaging (sMRI) thickness correlations were conducted across the sample and within patients and controls separately.During response inhibition (NoGo minus Go), bipolar subjects showed significant hypoactivation and reduced thickness in the inferior frontal cortex (IFC), superior frontal gyrus and cingulate compared to controls. Cingulate hypoactivation corresponded with reduced regional thickness. A significant activation by disease state interaction was observed with thickness in left prefrontal areas.Reduced cingulate fMRI activation is associated with reduced cortical thickness. In the left frontal lobe, a thinner cortex was associated with increased fMRI activation in patients, but showed a reverse trend in controls. These findings suggest that reduced activation in the IFC and cingulate during a response inhibition task may have an underlying structural etiology, which may explain task-related functional hypoactivation that persists even when patients are euthymic.

    View details for PubMedID 27990494

  • Sex differences in amygdala shape: Insights from Turner syndrome. Human brain mapping Green, T., Fierro, K. C., Raman, M. M., Foland-Ross, L., Hong, D. S., Reiss, A. L. 2016; 37 (4): 1593-1601

    Abstract

    Sex differences in the manifestation of psychiatric disorders, including anxiety disorders, are among the most prominent findings in psychiatry. The study of Turner syndrome (TS), caused by X-monosomy, has the potential to reveal mechanisms that underline male/female differences in neuropsychiatric disorders. The amygdala has been implicated in numerous neuropsychiatric disorders. Previous studies suggest an effect of TS on amygdala volume as well as on amygdala-related behaviors such as anxiety. Our objective is to investigate the amygdala shape in TS. Specifically, we tested whether amygdala enlargements in TS are localized to specific nuclei implicated in anxiety, such as the basomedial nucleus.We use a surface-based analytical modeling approach to contrast 41 pre-estrogen treatment girls with TS (mean age 8.6 ± 2.4) with 34 age-and sex-matched typically developing (TD) controls (mean age 8.0 ± 2.8). Anxiety symptoms were assessed using the Revised Children's Manifest Anxiety Scale - 2 (RCMAS-2) in both groups.TS was associated with anomalous enlargement of the amygdala. Surface-based modeling revealed shape differences (increased radial-distances) in bilateral basal and basomedial nuclei within the basolateral complex. RCMAS-2 Total Anxiety t-score was significantly higher in participants with TS compared with TD controls (P = 0.012).Group differences in global amygdala volumes were driven by local morphological increases in areas that are critically involved in face emotion processing and anxiety. In the context of increased amygdala volumes in TS, our results also showed increased worry and social anxiety in young girls with TS compared with TD. Hum Brain Mapp 37:1593-1601, 2016. © 2016 Wiley Periodicals, Inc.

    View details for DOI 10.1002/hbm.23122

    View details for PubMedID 26819071

  • Neural Aspects of Inhibition Following Emotional Primes in Depressed Adolescents. Journal of clinical child and adolescent psychology Colich, N. L., Foland-Ross, L. C., Eggleston, C., Singh, M. K., Gotlib, I. H. 2016; 45 (1): 21-30

    Abstract

    Adults diagnosed with major depressive disorder (MDD) have been found to be characterized by selective attention to negative material and by impairments in their ability to disengage from, or inhibit the processing of, negative stimuli. Altered functioning in the frontal executive control network has been posited to underlie these deficits in cognitive functioning. We know little, however, about the neural underpinnings of inhibitory difficulties in depressed adolescents. We used functional magnetic resonance imaging in 18 adolescents diagnosed with MDD and 15 age- and gender-matched healthy controls (CTLs) while they performed a modified affective Go/No-Go task that was designed to measure inhibitory control in the presence of an emotional distractor. Participants were presented with either a happy or a sad face, followed by a go or a no-go target to which they either made or inhibited a motor response. A group (MDD, CTL) by valence (happy, sad) by condition (go, no-go) analysis of variance indicated that MDD adolescents showed attenuated BOLD response in the right dorsolateral prefrontal cortex (DLPFC) and in the occipital cortex bilaterally, to no-go targets that followed a sad, but not a happy, face. Adolescents diagnosed with MDD showed anomalous recruitment of prefrontal control regions during inhibition trials, suggesting depression-associated disruption in neural underpinnings of the inhibition of emotional distractors. Given that the DLPFC is associated with the maintenance of goal-relevant information, it is likely that sad faces differentially capture attention in adolescents with MDD and interfere with task demands requiring inhibition.

    View details for DOI 10.1080/15374416.2014.982281

    View details for PubMedID 25635920

    View details for PubMedCentralID PMC4520793

  • Concordant Patterns of Brain Structure in Mothers with Recurrent Depression and Their Never-Depressed Daughters DEVELOPMENTAL NEUROSCIENCE Foland-Ross, L. C., Behzadian, N., LeMoult, J., Gotlib, I. H. 2016; 38 (2): 115-123

    Abstract

    A growing body of research has demonstrated that having a mother with a history of major depressive disorder (MDD) is one of the strongest predictors of depression in adolescent offspring. Few studies, however, have assessed neural markers of this increased risk for depression, or examined whether risk-related anomalies in adolescents at maternal risk for depression are related to neural abnormalities in their depressed mothers. We addressed these questions by examining concordance in brain structure in two groups of participants: mothers with a history of depression and their never-depressed daughters, and never-depressed mothers and their never-depressed daughters.We scanned mothers with (remitted; RMD) and without (control; CTL) a history of recurrent episodes of depression and their never-depressed daughters, computed cortical gray matter thickness, and tested whether mothers' thickness predicted daughters' thickness.Both RMD mothers and their high-risk daughters exhibited focal areas of thinner cortical gray matter compared with their CTL/low-risk counterparts. Importantly, the extent of thickness anomalies in RMD mothers predicted analogous abnormalities in their daughters; this pattern was not present in CTL/low-risk dyads.We identified neuroanatomical risk factors that may underlie the intergenerational transmission of risk for MDD. Our findings suggest that there is concordance in brain structure in dyads that is affected by maternal depression, and that the location, direction, and extent of neural anomalies in high-risk offspring mirror those of their recurrent depressed mothers.

    View details for DOI 10.1159/000444448

    View details for Web of Science ID 000379162600004

    View details for PubMedID 27198667

    View details for PubMedCentralID PMC4927380

  • Cortical thickness predicts the first onset of major depression in adolescence. International journal of developmental neuroscience Foland-Ross, L. C., Sacchet, M. D., Prasad, G., Gilbert, B., Thompson, P. M., Gotlib, I. H. 2015; 46: 125-131

    Abstract

    Given the increasing prevalence of Major Depressive Disorder and recent advances in preventative treatments for this disorder, an important challenge in pediatric neuroimaging is the early identification of individuals at risk for depression. We examined whether machine learning can be used to predict the onset of depression at the individual level. Thirty-three never-disordered adolescents (10-15 years old) underwent structural MRI. Participants were followed for 5 years to monitor the emergence of clinically significant depressive symptoms. We used support vector machines (SVMs) to test whether baseline cortical thickness could reliably distinguish adolescents who develop depression from adolescents who remained free of any Axis I disorder. Accuracies from subsampled cross-validated classification were used to assess classifier performance. Baseline cortical thickness correctly predicted the future onset of depression with an overall accuracy of 70% (69% sensitivity, 70% specificity; p=0.021). Examination of SVM feature weights indicated that the right medial orbitofrontal, right precentral, left anterior cingulate, and bilateral insular cortex contributed most strongly to this classification. These findings indicate that cortical gray matter structure can predict the subsequent onset of depression. An important direction for future research is to elucidate mechanisms by which these anomalies in gray matter structure increase risk for developing this disorder.

    View details for DOI 10.1016/j.ijdevneu.2015.07.007

    View details for PubMedID 26315399

  • Neural Markers of Familial Risk for Depression: An Investigation of Cortical Thickness Abnormalities in Healthy Adolescent Daughters of Mothers With Recurrent Depression JOURNAL OF ABNORMAL PSYCHOLOGY Foland-Ross, L. C., Gilbert, B. L., Joormann, J., Gotlib, I. H. 2015; 124 (3): 476-485

    Abstract

    Having a mother with major depressive disorder (MDD) is one of the strongest predictors of depression in late adolescence and early adulthood. Despite this fact, we know little about the neural mechanisms involved in the intergenerational transmission of risk for depression. Twenty-eight never-disordered daughters of recurrent depressed mothers (high-risk) and 36 never-disordered daughters of never-depressed mothers (low-risk) were scanned using MRI. Scan data were processed to provide measurements of cortical gray matter thickness. A general linear model was conducted at each surface point to assess the main effect of familial risk on cortical structure as well as to explore the interaction of familial risk and age. High-risk girls exhibited significantly thinner cortical gray matter in the right fusiform gyrus relative to low-risk girls. Exploratory analyses indicated interactions of risk group and age in the bilateral anterior insula and right anterior cingulate cortex (ACC); whereas low-risk girls exhibited an inverse association between age and thickness, girls at high risk for depression showed the reverse pattern. Additional exploratory analyses, using scores on the Children's Sadness Management Scale, indicated that thinner gray matter in the ACC of high-risk girls was associated with greater difficulty in managing sadness. These findings indicate that anomalous reductions in the cortical thickness of the fusiform gyrus may be a marker of risk for MDD. The interaction of age and group for gray matter thickness of the insula and ACC suggests a particularly important role for these regions in risk for depression and warrants additional research in longitudinal studies. (PsycINFO Database Record

    View details for DOI 10.1037/abn0000050

    View details for Web of Science ID 000359379000002

    View details for PubMedCentralID PMC4573777

  • Neural markers of familial risk for depression: An investigation of cortical thickness abnormalities in healthy adolescent daughters of mothers with recurrent depression. Journal of abnormal psychology Foland-Ross, L. C., Gilbert, B. L., Joormann, J., Gotlib, I. H. 2015; 124 (3): 476-485

    Abstract

    Having a mother with major depressive disorder (MDD) is one of the strongest predictors of depression in late adolescence and early adulthood. Despite this fact, we know little about the neural mechanisms involved in the intergenerational transmission of risk for depression. Twenty-eight never-disordered daughters of recurrent depressed mothers (high-risk) and 36 never-disordered daughters of never-depressed mothers (low-risk) were scanned using MRI. Scan data were processed to provide measurements of cortical gray matter thickness. A general linear model was conducted at each surface point to assess the main effect of familial risk on cortical structure as well as to explore the interaction of familial risk and age. High-risk girls exhibited significantly thinner cortical gray matter in the right fusiform gyrus relative to low-risk girls. Exploratory analyses indicated interactions of risk group and age in the bilateral anterior insula and right anterior cingulate cortex (ACC); whereas low-risk girls exhibited an inverse association between age and thickness, girls at high risk for depression showed the reverse pattern. Additional exploratory analyses, using scores on the Children's Sadness Management Scale, indicated that thinner gray matter in the ACC of high-risk girls was associated with greater difficulty in managing sadness. These findings indicate that anomalous reductions in the cortical thickness of the fusiform gyrus may be a marker of risk for MDD. The interaction of age and group for gray matter thickness of the insula and ACC suggests a particularly important role for these regions in risk for depression and warrants additional research in longitudinal studies. (PsycINFO Database Record

    View details for DOI 10.1037/abn0000050

    View details for PubMedID 25894441

  • HPA-axis reactivity interacts with stage of pubertal development to predict the onset of depression PSYCHONEUROENDOCRINOLOGY Colich, N. L., Kircanski, K., Foland-Ross, L. C., Gotlib, I. H. 2015; 55: 94-101

    Abstract

    Both elevated and blunted levels of cortisol secretion during childhood and adolescence have been linked to the subsequent onset of major depressive disorder (MDD). These mixed findings may be due to developmental changes in HPA-axis functioning, which have not been previously assessed in the context of risk. In the present study, therefore, we examined whether pubertal development moderated the influence of cortisol secretion on the subsequent development of MDD. Eighty-nine never-disordered girls ages 9-15 years, many of whom were at high risk for depression by virtue of having a maternal history of the disorder, completed a laboratory stress task. To index cortisol reactivity, salivary cortisol samples were collected at baseline and 15min following the onset of the stressor. Girls' levels of pubertal development were measured using Tanner staging. All participants were followed through age 18 in order to assess the subsequent development of MDD. Pubertal stage moderated the effects of cortisol stress reactivity on the development of MDD. Specifically, the onset of MDD was predicted by cortisol hyporeactivity in girls who were earlier in pubertal development (Tanner stage≤2), but by cortisol hyperreactivity in girls who were later in pubertal development (Tanner stage≥3.5).These findings demonstrate that girls' cortisol stress reactivity predicts the subsequent onset of MDD, and further, that the nature of this effect depends on the girls' level of pubertal development. Results are discussed in the context of clarifying previous findings, and directions for future research are offered.

    View details for DOI 10.1016/j.psyneuen.2015.02.004

    View details for Web of Science ID 000353090100009

    View details for PubMedCentralID PMC4380614

  • Concordance of mother-daughter diurnal cortisol production: Understanding the intergenerational transmission of risk for depression BIOLOGICAL PSYCHOLOGY LeMoult, J., Chen, M. C., Foland-Ross, L. C., Burley, H. W., Gotlib, I. H. 2015; 108: 98-104

    Abstract

    A growing body of research is demonstrating concordance between mother and child diurnal cortisol production. In the context of maternal history of depression, intergenerational concordance of cortisol production could contribute to hypercortisolemia in children of depressed mothers, which has been shown to increase risk for MDD. The current study is the first to examine concordance in diurnal cortisol production between mothers with a history of depression and their never-depressed, but high-risk, children. We collected salivary cortisol across 2 days from mothers with (remitted; RMD) and without (CTL) a history of recurrent episodes of depression and their never-depressed daughters. As expected, RMD mothers and their daughters both exhibited higher cortisol production than did their CTL counterparts. Moreover, both across and within groups, mothers' and daughters' cortisol production were directly coupled. These findings suggest that there is an intergenerational concordance in cortisol dysregulation that may contribute to hypercortisolemia in girls at familial risk for depression.

    View details for DOI 10.1016/j.biopsycho.2015.03.019

    View details for PubMedID 25862380

  • Telomere length and cortisol reactivity in children of depressed mothers. Molecular psychiatry Gotlib, I. H., LeMoult, J., Colich, N. L., Foland-Ross, L. C., Hallmayer, J., Joormann, J., Lin, J., Wolkowitz, O. M. 2015; 20 (5): 615-620

    Abstract

    A growing body of research demonstrates that individuals diagnosed with major depressive disorder (MDD) are characterized by shortened telomere length, which has been posited to underlie the association between depression and increased instances of medical illness. The temporal nature of the relation between MDD and shortened telomere length, however, is not clear. Importantly, both MDD and telomere length have been associated independently with high levels of stress, implicating dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis and anomalous levels of cortisol secretion in this relation. Despite these associations, no study has assessed telomere length or its relation with HPA-axis activity in individuals at risk for depression, before the onset of disorder. In the present study, we assessed cortisol levels in response to a laboratory stressor and telomere length in 97 healthy young daughters of mothers either with recurrent episodes of depression (i.e., daughters at familial risk for depression) or with no history of psychopathology. We found that daughters of depressed mothers had shorter telomeres than did daughters of never-depressed mothers and, further, that shorter telomeres were associated with greater cortisol reactivity to stress. This study is the first to demonstrate that children at familial risk of developing MDD are characterized by accelerated biological aging, operationalized as shortened telomere length, before they had experienced an onset of depression; this may predispose them to develop not only MDD but also other age-related medical illnesses. It is critical, therefore, that we attempt to identify and distinguish genetic and environmental mechanisms that contribute to telomere shortening.

    View details for DOI 10.1038/mp.2014.119

    View details for PubMedID 25266121

    View details for PubMedCentralID PMC4419149

  • Identification of a direct GABAergic pallidocortical pathway in rodents EUROPEAN JOURNAL OF NEUROSCIENCE Chen, M. C., Ferrari, L., Sacchet, M. D., Foland-Ross, L. C., Qiu, M., Gotlib, I. H., Fuller, P. M., Arrigoni, E., Lu, J. 2015; 41 (6): 748-759

    Abstract

    Interaction between the basal ganglia and the cortex plays a critical role in a range of behaviors. Output from the basal ganglia to the cortex is thought to be relayed through the thalamus, but an intriguing alternative is that the basal ganglia may directly project to and communicate with the cortex. We explored an efferent projection from the globus pallidus externa (GPe), a key hub in the basal ganglia system, to the cortex of rats and mice. Anterograde and retrograde tracing revealed projections to the frontal premotor cortex, especially the deep projecting layers, originating from GPe neurons that receive axonal inputs from the dorsal striatum. Cre-dependent anterograde tracing in Vgat-ires-cre mice confirmed that the pallidocortical projection is GABAergic, and in vitro optogenetic stimulation in the cortex of these projections produced a fast inhibitory postsynaptic current in targeted cells that was abolished by bicuculline. The pallidocortical projections targeted GABAergic interneurons and, to a lesser extent, pyramidal neurons. This GABAergic pallidocortical pathway directly links the basal ganglia and cortex, and may play a key role in behavior and cognition in normal and disease states.

    View details for DOI 10.1111/ejn.12822

    View details for Web of Science ID 000351439000002

    View details for PubMedID 25581560

    View details for PubMedCentralID PMC4363158

  • Support vector machine classification of major depressive disorder using diffusion-weighted neuroimaging and graph theory FRONTIERS IN PSYCHIATRY Sacchet, M. D., Prasad, G., Foland-Ross, L. C., Thompson, P. M., Gotlib, I. H. 2015; 6

    Abstract

    Recently, there has been considerable interest in understanding brain networks in major depressive disorder (MDD). Neural pathways can be tracked in the living brain using diffusion-weighted imaging (DWI); graph theory can then be used to study properties of the resulting fiber networks. To date, global abnormalities have not been reported in tractography-based graph metrics in MDD, so we used a machine learning approach based on "support vector machines" to differentiate depressed from healthy individuals based on multiple brain network properties. We also assessed how important specific graph metrics were for this differentiation. Finally, we conducted a local graph analysis to identify abnormal connectivity at specific nodes of the network. We were able to classify depression using whole-brain graph metrics. Small-worldness was the most useful graph metric for classification. The right pars orbitalis, right inferior parietal cortex, and left rostral anterior cingulate all showed abnormal network connectivity in MDD. This is the first use of structural global graph metrics to classify depressed individuals. These findings highlight the importance of future research to understand network properties in depression across imaging modalities, improve classification results, and relate network alterations to psychiatric symptoms, medication, and comorbidities.

    View details for DOI 10.3389/fpsyt.2015.00021

    View details for Web of Science ID 000364204500001

    View details for PubMedCentralID PMC4332161

  • Support vector machine classification of major depressive disorder using diffusion-weighted neuroimaging and graph theory. Frontiers in psychiatry Sacchet, M. D., Prasad, G., Foland-Ross, L. C., Thompson, P. M., Gotlib, I. H. 2015; 6: 21-?

    Abstract

    Recently, there has been considerable interest in understanding brain networks in major depressive disorder (MDD). Neural pathways can be tracked in the living brain using diffusion-weighted imaging (DWI); graph theory can then be used to study properties of the resulting fiber networks. To date, global abnormalities have not been reported in tractography-based graph metrics in MDD, so we used a machine learning approach based on "support vector machines" to differentiate depressed from healthy individuals based on multiple brain network properties. We also assessed how important specific graph metrics were for this differentiation. Finally, we conducted a local graph analysis to identify abnormal connectivity at specific nodes of the network. We were able to classify depression using whole-brain graph metrics. Small-worldness was the most useful graph metric for classification. The right pars orbitalis, right inferior parietal cortex, and left rostral anterior cingulate all showed abnormal network connectivity in MDD. This is the first use of structural global graph metrics to classify depressed individuals. These findings highlight the importance of future research to understand network properties in depression across imaging modalities, improve classification results, and relate network alterations to psychiatric symptoms, medication, and comorbidities.

    View details for DOI 10.3389/fpsyt.2015.00021

    View details for PubMedID 25762941

    View details for PubMedCentralID PMC4332161

  • Coping with having a depressed mother: The role of stress and coping in hypothalamic-pituitary-adrenal axis dysfunction in girls at familial risk for major depression DEVELOPMENT AND PSYCHOPATHOLOGY Foland-Ross, L. C., Kircanski, K., Gotlib, I. H. 2014; 26 (4): 1401-1409

    Abstract

    Having a depressed mother is one of the strongest predictors of depression in adolescence. We investigated whether the stress of having a mother with recurrent depression is associated with dysfunction in adolescents in the HPA axis and whether the tendency to use involuntary coping strategies in dealing with this stress is associated with exacerbation of dysfunction in this system. Sixty-four never-disordered daughters of mothers with recurrent depression (high risk) and 64 never-disordered daughters of never-disordered mothers (low risk) completed diurnal cortisol and stress assessments. High-risk girls secreted more diurnal cortisol than did low-risk girls. Whereas low-risk girls secreted higher levels of cortisol with increasing stress associated with having a depressed mother, no such relation was present in high-risk girls. Finally, in contrast to low-risk girls, girls at familial risk for depression who more frequently used involuntary versus voluntary coping exhibited the greatest elevations in diurnal cortisol. These findings indicate that a tendency to utilize involuntary, as opposed to voluntary, coping strategies in dealing with stress involving maternal depression exacerbates already high levels of cortisol in youth at risk for depression. Future research that examines whether interventions aimed at increasing the use of voluntary coping strategies normalizes HPA axis dysfunction is of interest.

    View details for DOI 10.1017/S0954579414001102

    View details for Web of Science ID 000345576500016

  • Coping with having a depressed mother: the role of stress and coping in hypothalamic-pituitary-adrenal axis dysfunction in girls at familial risk for major depression. Development and psychopathology Foland-Ross, L. C., Kircanski, K., Gotlib, I. H. 2014; 26 (4): 1401-1409

    Abstract

    Having a depressed mother is one of the strongest predictors of depression in adolescence. We investigated whether the stress of having a mother with recurrent depression is associated with dysfunction in adolescents in the HPA axis and whether the tendency to use involuntary coping strategies in dealing with this stress is associated with exacerbation of dysfunction in this system. Sixty-four never-disordered daughters of mothers with recurrent depression (high risk) and 64 never-disordered daughters of never-disordered mothers (low risk) completed diurnal cortisol and stress assessments. High-risk girls secreted more diurnal cortisol than did low-risk girls. Whereas low-risk girls secreted higher levels of cortisol with increasing stress associated with having a depressed mother, no such relation was present in high-risk girls. Finally, in contrast to low-risk girls, girls at familial risk for depression who more frequently used involuntary versus voluntary coping exhibited the greatest elevations in diurnal cortisol. These findings indicate that a tendency to utilize involuntary, as opposed to voluntary, coping strategies in dealing with stress involving maternal depression exacerbates already high levels of cortisol in youth at risk for depression. Future research that examines whether interventions aimed at increasing the use of voluntary coping strategies normalizes HPA axis dysfunction is of interest.

    View details for DOI 10.1017/S0954579414001102

    View details for PubMedID 25422969

  • Recalling happy memories in remitted depression: A neuroimaging investigation of the repair of sad mood COGNITIVE AFFECTIVE & BEHAVIORAL NEUROSCIENCE Foland-Ross, L. C., Cooney, R. E., Joormann, J., Henry, M. L., Gotlib, I. H. 2014; 14 (2): 818-826

    Abstract

    Major depressive disorder (MDD) is a recurrent mood disorder. The high rate of recurrence of MDD suggests the presence of stable vulnerability factors that place individuals with a history of major depression at an increased risk for the onset of another episode. Previous research has linked the remitted state, and therefore increased vulnerability for depressive relapse, with difficulties in the use of pleasant autobiographical memories to repair sad mood. In the present study, we examined the neural correlates of these difficulties. Groups of 16 currently euthymic, remitted depressed individuals and 16 healthy (control) women underwent functional magnetic resonance imaging (fMRI) during sad mood induction and during recovery from a sad mood state through recall of mood-incongruent positive autobiographical memories. Sad mood was induced in participants by using film clips; participants then recalled positive autobiographical memories, a procedure previously shown to repair negative affect. During both the sad mood induction and automatic mood regulation, control participants exhibited activation in the left ventrolateral prefrontal cortex (vlPFC) and cuneus; in contrast, remitted participants exhibited a decrease in activation in these regions. Furthermore, exploratory analyses revealed that reduced activation levels during mood regulation predicted a worsening of depressive symptoms at a 20-month follow-up assessment. These findings highlight a dynamic role of the vlPFC and cuneus in the experience and modulation of emotional states and suggest that functional anomalies of these brain regions are associated with a history of, and vulnerability to, depression.

    View details for DOI 10.3758/s13415-013-0216-0

    View details for Web of Science ID 000338516800026

    View details for PubMedCentralID PMC3995858

  • Recalling happy memories in remitted depression: a neuroimaging investigation of the repair of sad mood. Cognitive, affective & behavioral neuroscience Foland-Ross, L. C., Cooney, R. E., Joormann, J., Henry, M. L., Gotlib, I. H. 2014; 14 (2): 818-826

    Abstract

    Major depressive disorder (MDD) is a recurrent mood disorder. The high rate of recurrence of MDD suggests the presence of stable vulnerability factors that place individuals with a history of major depression at an increased risk for the onset of another episode. Previous research has linked the remitted state, and therefore increased vulnerability for depressive relapse, with difficulties in the use of pleasant autobiographical memories to repair sad mood. In the present study, we examined the neural correlates of these difficulties. Groups of 16 currently euthymic, remitted depressed individuals and 16 healthy (control) women underwent functional magnetic resonance imaging (fMRI) during sad mood induction and during recovery from a sad mood state through recall of mood-incongruent positive autobiographical memories. Sad mood was induced in participants by using film clips; participants then recalled positive autobiographical memories, a procedure previously shown to repair negative affect. During both the sad mood induction and automatic mood regulation, control participants exhibited activation in the left ventrolateral prefrontal cortex (vlPFC) and cuneus; in contrast, remitted participants exhibited a decrease in activation in these regions. Furthermore, exploratory analyses revealed that reduced activation levels during mood regulation predicted a worsening of depressive symptoms at a 20-month follow-up assessment. These findings highlight a dynamic role of the vlPFC and cuneus in the experience and modulation of emotional states and suggest that functional anomalies of these brain regions are associated with a history of, and vulnerability to, depression.

    View details for DOI 10.3758/s13415-013-0216-0

    View details for PubMedID 24146315

  • CHARACTERIZING WHITE MATTER CONNECTIVITY IN MAJOR DEPRESSIVE DISORDER: AUTOMATED FIBER QUANTIFICATION AND MAXIMUM DENSITY PATHS. Proceedings. IEEE International Symposium on Biomedical Imaging Sacchet, M. D., Prasad, G., Foland-Ross, L. C., Joshi, S. H., Hamilton, J. P., Thompson, P. M., Gotlib, I. H. 2014; 11: 592-595

    Abstract

    Diffusion-weighted imaging allows for in vivo assessment of white matter structure, which can be used to assess aberrations associated with disease. Several new methods permit the automated assessment of important white matter characteristics. In the current study we used Automated Fiber Quantification (AFQ) to assess differences between depressed and nondepressed individuals in 18 major white matter tracts. We then used the Maximum Density Path (MDP) method to further characterize group differences identified with AFQ. The results of the AFQ analyses indicated that fractional anisotropy (FA; an index of white matter integrity) along bilateral corticospinal tracts (CST) was higher in depressed than in nondepressed individuals. MDP analyses revealed that white matter anomalies were restricted to four subregions that included the corona radiata and the internal and external capsules. These results provide further evidence that MDD is associated with abnormalities in cortical-to-subcortical connectivity.

    View details for PubMedID 25540677

  • ELUCIDATING BRAIN CONNECTIVITY NETWORKS IN MAJOR DEPRESSIVE DISORDER USING CLASSIFICATION-BASED SCORING. Proceedings. IEEE International Symposium on Biomedical Imaging Sacchet, M. D., Prasad, G., Foland-Ross, L. C., Thompson, P. M., Gotlib, I. H. 2014; 2014: 246-249

    Abstract

    Graph theory is increasingly used in the field of neuroscience to understand the large-scale network structure of the human brain. There is also considerable interest in applying machine learning techniques in clinical settings, for example, to make diagnoses or predict treatment outcomes. Here we used support-vector machines (SVMs), in conjunction with whole-brain tractography, to identify graph metrics that best differentiate individuals with Major Depressive Disorder (MDD) from nondepressed controls. To do this, we applied a novel feature-scoring procedure that incorporates iterative classifier performance to assess feature robustness. We found that small-worldness, a measure of the balance between global integration and local specialization, most reliably differentiated MDD from nondepressed individuals. Post-hoc regional analyses suggested that heightened connectivity of the subcallosal cingulate gyrus (SCG) in MDDs contributes to these differences. The current study provides a novel way to assess the robustness of classification features and reveals anomalies in large-scale neural networks in MDD.

    View details for PubMedID 25580184

  • Activation of the medial prefrontal and posterior cingulate cortex during encoding of negative material predicts symptom worsening in major depression. Neuroreport Foland-Ross, L. C., Hamilton, P., Sacchet, M. D., Furman, D. J., Sherdell, L., Gotlib, I. H. 2014; 25 (5): 324-329

    Abstract

    Considerable research indicates that depressed individuals have better memory for negative material than do nondepressed individuals, and that this bias is associated with differential patterns of neural activation. It is not known, however, whether these aberrant activation patterns predict illness course. Using functional neuroimaging, we examined whether change in depressive symptoms is predicted by baseline patterns of neural activation that underlie negative memory biases in major depressive disorder. Depressed participants viewed negative and neutral pictures during functional MRI at baseline and completed an incidental memory task for these pictures 1 week later. Depression severity was assessed by administering the Beck Depression Inventory both at baseline (Time 1) and at Time 2, an average of 18 months later. Contrast maps of activation for subsequently remembered negative versus subsequently remembered neutral pictures were regressed against change in Beck Depression Inventory scores between Time 1 and Time 2, controlling for initial symptom severity. Results from this analysis revealed no associations between memory sensitivity for negative stimuli and symptom change. In contrast, whole brain analyses revealed significant positive associations between within-subject changes in depressive symptoms and baseline neural activation to successfully recalled negative pictures in the posterior cingulate cortex and medial prefrontal cortex. These findings indicate that neural activation in cortical midline regions is a better predictor of long-term symptomatic outcome than is memory sensitivity for negative material.

    View details for DOI 10.1097/WNR.0000000000000095

    View details for PubMedID 24356105

    View details for PubMedCentralID PMC3947655

  • Understanding Familial Risk for Depression: A 25-Year Perspective PERSPECTIVES ON PSYCHOLOGICAL SCIENCE Gotlib, I. H., Joormann, J., Foland-Ross, L. C. 2014; 9 (1): 94-108

    Abstract

    Major depressive disorder (MDD) is among the most prevalent, debilitating, and costly of all illnesses worldwide. Investigators have made considerable progress in elucidating psychological and biological correlates of MDD; however, far less is known about factors that are implicated in risk for depression. Given the high risk for MDD associated with a family history of depression, investigators have worked to understand both the effects of parental depression on offspring and the mechanisms that might underlie familial risk for MDD. In this article, we describe the evolution of investigators' understanding of the psychobiological functioning of children of depressed parents, and we present recent findings concerning cognitive and neural aspects of risk for MDD using our high-risk sample as a context and foundation for this discussion. We integrate these data in a conceptualization of mechanisms underlying risk for depression, focusing on the constructs of emotion dysregulation and stress reactivity. Recognizing the 25-year anniversary of the Association for Psychological Science, we place this presentation in the context of the past 25 years of research on depression. We conclude by discussing the significance of emotion dysregulation and stress reactivity for studying risk for depression, for developing approaches to prevent MDD, and for moving theory and research in this field forward.

    View details for DOI 10.1177/1745691613513469

    View details for Web of Science ID 000330848700013

  • Understanding Familial Risk for Depression: A 25-Year Perspective. Perspectives on psychological science Gotlib, I. H., Joormann, J., Foland-Ross, L. C. 2014; 9 (1): 94-108

    Abstract

    Major depressive disorder (MDD) is among the most prevalent, debilitating, and costly of all illnesses worldwide. Investigators have made considerable progress in elucidating psychological and biological correlates of MDD; however, far less is known about factors that are implicated in risk for depression. Given the high risk for MDD associated with a family history of depression, investigators have worked to understand both the effects of parental depression on offspring and the mechanisms that might underlie familial risk for MDD. In this article, we describe the evolution of investigators' understanding of the psychobiological functioning of children of depressed parents, and we present recent findings concerning cognitive and neural aspects of risk for MDD using our high-risk sample as a context and foundation for this discussion. We integrate these data in a conceptualization of mechanisms underlying risk for depression, focusing on the constructs of emotion dysregulation and stress reactivity. Recognizing the 25-year anniversary of the Association for Psychological Science, we place this presentation in the context of the past 25 years of research on depression. We conclude by discussing the significance of emotion dysregulation and stress reactivity for studying risk for depression, for developing approaches to prevent MDD, and for moving theory and research in this field forward.

    View details for DOI 10.1177/1745691613513469

    View details for PubMedID 26173248

  • Structural abnormality of the corticospinal tract in major depressive disorder. Biology of mood & anxiety disorders Sacchet, M. D., Prasad, G., Foland-Ross, L. C., Joshi, S. H., Hamilton, J. P., Thompson, P. M., Gotlib, I. H. 2014; 4: 8-?

    Abstract

    Scientists are beginning to document abnormalities in white matter connectivity in major depressive disorder (MDD). Recent developments in diffusion-weighted image analyses, including tractography clustering methods, may yield improved characterization of these white matter abnormalities in MDD. In this study, we acquired diffusion-weighted imaging data from MDD participants and matched healthy controls. We analyzed these data using two tractography clustering methods: automated fiber quantification (AFQ) and the maximum density path (MDP) procedure. We used AFQ to compare fractional anisotropy (FA; an index of water diffusion) in these two groups across major white matter tracts. Subsequently, we used the MDP procedure to compare FA differences in fiber paths related to the abnormalities in major fiber tracts that were identified using AFQ.FA was higher in the bilateral corticospinal tracts (CSTs) in MDD (p's < 0.002). Secondary analyses using the MDP procedure detected primarily increases in FA in the CST-related fiber paths of the bilateral posterior limbs of the internal capsule, right superior corona radiata, and the left external capsule.This is the first study to implicate the CST and several related fiber pathways in MDD. These findings suggest important new hypotheses regarding the role of CST abnormalities in MDD, including in relation to explicating CST-related abnormalities to depressive symptoms and RDoC domains and constructs.

    View details for DOI 10.1186/2045-5380-4-8

    View details for PubMedID 25295159

    View details for PubMedCentralID PMC4187017

  • The Neural Basis of Difficulties Disengaging From Negative Irrelevant Material in Major Depression PSYCHOLOGICAL SCIENCE Foland-Ross, L. C., Hamilton, J. P., Joormann, J., Berman, M. G., Jonides, J., Gotlib, I. H. 2013; 24 (3): 334-344

    Abstract

    Recurrent uncontrollable negative thoughts are a hallmark of depressive episodes. Deficits in cognitive control have been proposed to underlie this debilitating aspect of depression. Here, we used functional neuroimaging during an emotional working memory (WM) task to elucidate the neural correlates of these difficulties in cognitive control. In a WM manipulation involving depressed participants, the dorsal anterior cingulate and parietal and bilateral insular cortices were activated significantly more when negative words were removed from WM than when they were maintained in WM; in contrast, nondepressed participants exhibited stronger neural activations in these regions for positive than for negative material. These findings implicate anomalous activation of components of the task-positive network, known to be modulated by cognitive effort, in depression-associated difficulties in expelling negative material from WM. Future studies should examine the association between these aberrations and the maintenance of depressive symptoms.

    View details for DOI 10.1177/0956797612457380

    View details for Web of Science ID 000316640900014

    View details for PubMedID 23334445

  • Neurobiological markers of familial risk for depression. Current topics in behavioral neurosciences Foland-Ross, L. C., Hardin, M. G., Gotlib, I. H. 2013; 14: 181-206

    Abstract

    Major depression is associated with a wide range of neurobiological disturbances, including anomalies in the structure and function of cortical and subcortical gray matter and dysregulation of the HPA axis. In this chapter, we review research demonstrating that many of these abnormalities are also present in never-depressed offspring of adults with recurrent depression and discuss how such findings might reflect dysfunctional neuroregulatory systems that precede the onset of this disorder. We also briefly discuss candidate genes and environmental factors that have been posited to be directly involved in the transmission of neural and HPA-axis abnormalities from depressed parents to their offspring, and we review how, by obtaining a better understanding of the neurobiological markers of depression risk, we can facilitate the development of targeted strategies for the prevention and treatment of major depression.

    View details for DOI 10.1007/7854_2012_213

    View details for PubMedID 22573472

  • ADHD comorbidity can matter when assessing cortical thickness abnormalities in patients with bipolar disorder BIPOLAR DISORDERS Hegarty, C. E., Foland-Ross, L. C., Narr, K. L., Sugar, C. A., McGough, J. J., Thompson, P. M., Altshuler, L. L. 2012; 14 (8): 843-855

    Abstract

    Attention-deficit hyperactivity disorder (ADHD) is prevalent in patients with bipolar disorder (BP), but very few studies consider this when interpreting magnetic resonance imaging findings. No studies, to our knowledge, have screened for or controlled for the presence of ADHD when examining cortical thickness in patients with BP. We used a 2 × 2 design to evaluate the joint effects of BP and ADHD on cortical thickness and uncover the importance of ADHD comorbidity in BP subjects.The study included 85 subjects: 31 healthy controls, 17 BP-only, 19 ADHD-only, and 18 BP/ADHD. All patients with BP were subtype I, euthymic, and not taking lithium. Groups did not differ significantly in age or gender distribution. We used cortical thickness measuring tools combined with cortical pattern matching methods to align sulcal/gyral anatomy across participants. Significance maps were used to check for both main effects of BP and ADHD and their interaction. Post-hoc comparisons assessed how the effects of BP on cortical thickness varied as a function of the presence or absence of ADHD.Interactions of BP and ADHD diagnoses were found in the left subgenual cingulate and right orbitofrontal cortex, demonstrating that the effect of BP on cortical thickness depends on ADHD status.Some brain abnormalities attributed to BP may result from the presence of ADHD. Diagnostic interactions were found in regions previously implicated in the pathophysiology of BP, making it vital to control for an ADHD comorbid diagnosis when attempting to isolate neural or genetic abnormalities specific to BP.

    View details for DOI 10.1111/bdi.12024

    View details for Web of Science ID 000311403600006

    View details for PubMedID 23167934

  • Deficits in inferior frontal cortex activation in euthymic bipolar disorder patients during a response inhibition task BIPOLAR DISORDERS Townsend, J. D., Bookheimer, S. Y., Foland-Ross, L. C., Moody, T. D., Eisenberger, N. I., Fischer, J. S., Cohen, M. S., Sugar, C. A., Altshuler, L. L. 2012; 14 (4): 442-450

    Abstract

    The inferior frontal cortical-striatal network plays an integral role in response inhibition in normal populations. While inferior frontal cortex (IFC) impairment has been reported in mania, this study explored whether this dysfunction persists in euthymia.Functional magnetic resonance imaging (fMRI) activation was evaluated in 32 euthymic patients with bipolar I disorder and 30 healthy subjects while performing the Go/NoGo response inhibition task. Behavioral data were collected to evaluate accuracy and response time. Within-group and between-group comparisons of activation were conducted using whole-brain analyses to probe significant group differences in neural function.Both groups activated bilateral IFC. However, between-group comparisons showed a significantly reduced activation in this brain region in euthymic patients with bipolar disorder compared to healthy subjects. Other frontal and basal ganglia regions involved in response inhibition were additionally significantly reduced in bipolar disorder patients, in both the medicated and the unmedicated subgroups. No areas of greater activation were observed in bipolar disorder patients versus healthy subjects.Bipolar disorder patients, even during euthymia, have a persistent reduction in activation of brain regions involved in response inhibition, suggesting that reduced activation in the orbitofrontal cortex and striatum is not solely related to the state of mania. These findings may represent underlying trait abnormalities in bipolar disorder.

    View details for DOI 10.1111/j.1399-5618.2012.01020.x

    View details for Web of Science ID 000304441200008

    View details for PubMedID 22631623

  • Anterior cingulate activation relates to local cortical thickness NEUROREPORT Hegarty, C. E., Foland-Ross, L. C., Narr, K. L., Townsend, J. D., Bookheimer, S. Y., Thompson, P. M., Altshuler, L. L. 2012; 23 (7): 420-424

    Abstract

    Few studies have examined the relationship between local anatomic thickness of the cortex and the activation signals arising from it. Using structural and functional MRI, we examined whether a relationship exists between cortical thickness and brain activation. Twenty-eight participants were asked to perform the Go/NoGo response inhibition task known to activate the anterior cingulate and the prefrontal cortex. Structural data of the same regions were simultaneously collected. We hypothesized that cortical thickness in these brain regions would positively correlate with brain activation. Data from the structural MRI were aligned with those of functional MRI activation. There was a positive linear correlation between cortical thickness and activation during response inhibition in the right anterior cingulate cortex (Brodmann's Area 24). No significant thickness-activation correlations were found in the prefrontal cortex. Correlations between cortical thickness and activation may occur only in certain brain regions.

    View details for DOI 10.1097/WNR.0b013e3283525a95

    View details for Web of Science ID 000302948500003

    View details for PubMedID 22440976

  • Cognitive and neural aspects of information processing in major depressive disorder: an integrative perspective. Frontiers in psychology Foland-Ross, L. C., Gotlib, I. H. 2012; 3: 489-?

    Abstract

    Researchers using experimental paradigms to examine cognitive processes have demonstrated that Major Depressive Disorder (MDD) is associated not with a general deficit in cognitive functioning, but instead with more specific anomalies in the processing of negatively valenced material. Indeed, cognitive theories of depression posit that negative biases in the processing of information play a critical role in influencing the onset, maintenance, and recurrence of depressive episodes. In this paper we review findings from behavioral studies documenting that MDD is associated with specific difficulties in attentional disengagement from negatively valenced material, with tendencies to interpret information in a negative manner, with deficits in cognitive control in the processing of negative material, and with enhanced memory for negative material. To gain a better understanding of the neurobiological basis of these abnormalities, we also examine findings from functional neuroimaging studies of depression and show that dysfunction in neural systems that subserve emotion processing, inhibition, and attention may underlie and contribute to the deficits in cognition that have been documented in depressed individuals. Finally, we briefly review evidence from studies of children who are at high familial risk for depression that indicates that abnormalities in cognition and neural function are observable before the onset of MDD and, consequently, may represent a risk factor for the development of this disorder. By integrating research from cognitive and neural investigations of depression, we can gain a more comprehensive understanding not only of how cognitive and biological factors interact to affect the onset, maintenance, and course of MDD, but also of how such research can aid in the development of targeted strategies for the prevention and treatment of this debilitating disorder.

    View details for DOI 10.3389/fpsyg.2012.00489

    View details for PubMedID 23162521

    View details for PubMedCentralID PMC3495336

  • Cognitive and neural aspects of information processing in major depressive disorder: an integrative perspective FRONTIERS IN PSYCHOLOGY Foland-Ross, L. C., Gotlib, I. H. 2012; 3

    Abstract

    Researchers using experimental paradigms to examine cognitive processes have demonstrated that Major Depressive Disorder (MDD) is associated not with a general deficit in cognitive functioning, but instead with more specific anomalies in the processing of negatively valenced material. Indeed, cognitive theories of depression posit that negative biases in the processing of information play a critical role in influencing the onset, maintenance, and recurrence of depressive episodes. In this paper we review findings from behavioral studies documenting that MDD is associated with specific difficulties in attentional disengagement from negatively valenced material, with tendencies to interpret information in a negative manner, with deficits in cognitive control in the processing of negative material, and with enhanced memory for negative material. To gain a better understanding of the neurobiological basis of these abnormalities, we also examine findings from functional neuroimaging studies of depression and show that dysfunction in neural systems that subserve emotion processing, inhibition, and attention may underlie and contribute to the deficits in cognition that have been documented in depressed individuals. Finally, we briefly review evidence from studies of children who are at high familial risk for depression that indicates that abnormalities in cognition and neural function are observable before the onset of MDD and, consequently, may represent a risk factor for the development of this disorder. By integrating research from cognitive and neural investigations of depression, we can gain a more comprehensive understanding not only of how cognitive and biological factors interact to affect the onset, maintenance, and course of MDD, but also of how such research can aid in the development of targeted strategies for the prevention and treatment of this debilitating disorder.

    View details for DOI 10.3389/fpsyg.2012.00489

    View details for Web of Science ID 000208864000198

    View details for PubMedCentralID PMC3495336