Dr. Ordaz received her PhD in Clinical and Developmental Psychology from the University of Pittsburgh, completed her child clinical internship at the University of Washington, and completed her postdoctoral training at Stanford University. Her research explores the emergence of depression in adolescence by examining processes of developmental change in biomarkers of emotional reactivity and regulation, including brain structure and function.

Honors & Awards

  • NARSAD Young Investigator Award, Brain & Behavior Foundation (2016-)
  • K01 Award, NIMH (2015-)
  • Klingenstein Third Generation Foundation Fellowship Award, Klingenstein Third Generation Foundation (2014-)
  • T32 Clinical Research Fellowship, Stanford University (2013-2015)
  • CNI Seed Grant Award, Stanford Center for Cognitive and Neurobiological Imaging (2013-2014)
  • Graduate Research Fellowship Program, National Science Foundation (2007-2011)
  • K. Leroy Irvis Fellowship, University of Pittsburgh (2006-2007, 2011-2012)

Professional Education

  • Postdoc, Stanford University, Psychology (2015)
  • Internship, University of Washington, Child Clinical Psychology (2013)
  • Ph.D., University of Pittsburgh, Clinical and Developmental Psychology (2013)
  • B.S., Duke University, Psychology (2002)

Research & Scholarship

Current Research and Scholarly Interests

My research seeks to understand three fundamental questions: First, how do trajectories of brain development go awry in youth who become depressed? Second, how is maladaptive brain development perpetuated or worsened over the course of a depressive episode? Third, how might positive parenting buffer against maladaptive trajectories?

In one study, we have recruited early-pubertal girls who will be scanned (structural and functional neuroimaging) five times over the course of their pubertal maturation. We will investigate when and how brain network development goes off-course in girls who become depressed, how pubertal hormones might contribute to this, and how positive parenting might buffer against maladaptive trajectories. This work is being done in collaboration with Ian Gotlib and is funded by an NIMH K01 award.

A second study is a longitudinal neuroimaging study of currently-depressed teens. Teens come to the lab twice over the course of six months; at each visit we characterize their clinical symptomatology, obtain structural and functional neuroimaging scans, and assess parenting behavior. We will examine whether the known relationship between positive parenting and clinical course of depression is mediated by rates of change in connectivity among networks implicated in emotional reactivity, rumination, and emotion regulation. This work is a collaboration with Manpreet Singh and Ian Gotlib, and it is funded by a NARSAD Young Investigator Award and a Klingenstein Third Generation Foundation Award.


2016-17 Courses


All Publications

  • Investigating the nature of co-occurring depression and anxiety: Comparing diagnostic and dimensional research approaches. Journal of affective disorders Kircanski, K., LeMoult, J., Ordaz, S., Gotlib, I. H. 2016


    Although approximately half of adults diagnosed with a depressive or anxiety disorder exhibit their simultaneous co-occurrence, traditional research has centered on single-target diagnoses, overlooking comorbidities within samples. In this article, we review and extend the literature that directly investigates co-occurring depression and anxiety, with the goal of shifting the focus from co-occurring diagnoses to symptom dimensions.First, we review studies that have directly compared psychobiological features (neural, neuroendocrine, autonomic) across depression, anxiety, and their co-occurrence, defined either categorically or dimensionally. Second, we analyze adults' diurnal cortisol secretion to examine the independent and interactive relations of continuously-assessed depressive and anxiety symptoms to neuroendocrine function.Previous findings on the psychobiology of diagnostic co-occurrence are mixed. While nascent, evidence from dimensionally focused studies suggests that co-occurring levels of depressive and anxiety symptoms can interact with one another, as reflected in a distinct psychobiological profile for individuals with high levels of both symptom dimensions. Results of our analyses support this formulation: we found that depressive and anxiety symptom dimensions interacted consistently in their relation to the measures of diurnal cortisol.The illustrative sample was relatively small and included only women; future research should examine generalizability of these findings.A dimensional approach to investigating the psychobiology of co-occurring depression and anxiety affords both conceptual and practical advantages. Simultaneously assessing depressive and anxiety symptom dimensions can efficiently capture their unique, shared, and interactive features, thereby identifying targets for intervention across a wide range of symptom presentations.

    View details for DOI 10.1016/j.jad.2016.08.006

    View details for PubMedID 27554605

  • The Importance of Assessing Neural Trajectories in Pediatric Depression JAMA PSYCHIATRY Gotlib, I. H., Ordaz, S. J. 2016; 73 (1): 9-10
  • Predicting First Onset of Depression in Young Girls: Interaction of Diurnal Cortisol and Negative Life Events JOURNAL OF ABNORMAL PSYCHOLOGY LeMoult, J., Ordaz, S. J., Kircanski, K., Singh, M. K., Gotlib, I. H. 2015; 124 (4): 850-859

    View details for DOI 10.1037/abn0000087

    View details for Web of Science ID 000365609000007

  • Longitudinal Growth Curves of Brain Function Underlying Inhibitory Control through Adolescence JOURNAL OF NEUROSCIENCE Ordaz, S. J., Foran, W., Velanova, K., Luna, B. 2013; 33 (46): 18109-18124


    Neuroimaging studies suggest that developmental improvements in inhibitory control are primarily supported by changes in prefrontal executive function. However, studies are contradictory with respect to how activation in prefrontal regions changes with age, and they have yet to analyze longitudinal data using growth curve modeling, which allows characterization of dynamic processes of developmental change, individual differences in growth trajectories, and variables that predict any interindividual variability in trajectories. In this study, we present growth curves modeled from longitudinal fMRI data collected over 302 visits (across ages 9 to 26 years) from 123 human participants. Brain regions within circuits known to support motor response control, executive control, and error processing (i.e., aspects of inhibitory control) were investigated. Findings revealed distinct developmental trajectories for regions within each circuit and indicated that a hierarchical pattern of maturation of brain activation supports the gradual emergence of adult-like inhibitory control. Mean growth curves of activation in motor response control regions revealed no changes with age, although interindividual variability decreased with development, indicating equifinality with maturity. Activation in certain executive control regions decreased with age until adolescence, and variability was stable across development. Error-processing activation in the dorsal anterior cingulate cortex showed continued increases into adulthood and no significant interindividual variability across development, and was uniquely associated with task performance. These findings provide evidence that continued maturation of error-processing abilities supports the protracted development of inhibitory control over adolescence, while motor response control regions provide early-maturing foundational capacities and suggest that some executive control regions may buttress immature networks as error processing continues to mature.

    View details for DOI 10.1523/JNEUROSCI.1741-13.2013

    View details for Web of Science ID 000327020600014

    View details for PubMedID 24227721

  • Sex differences in physiological reactivity to acute psychosocial stress in adolescence PSYCHONEUROENDOCRINOLOGY Ordaz, S., Luna, B. 2012; 37 (8): 1135-1157


    Females begin to demonstrate greater negative affective responses to stress than males in adolescence. This may reflect the concurrent emergence of underlying differences in physiological response systems, including corticolimbic circuitries, the hypothalamic-pituitary-adrenal axis (HPAA), and the autonomic nervous system (ANS). This review examines when sex differences in physiological reactivity to acute psychosocial stress emerge and the directionality of these differences over development. Indeed, the literature indicates that sex differences emerge during adolescence and persist into adulthood for all three physiological response systems. However, the directionality of the differences varies by system. The emerging corticolimbic reactivity literature suggests greater female reactivity, particularly in limbic regions densely innervated by gonadal hormone receptors. In contrast, males generally show higher levels of HPAA and ANS reactivity. We argue that the contrasting directionality of corticolimbic and peripheral physiological responses may reflect specific effects of gonadal hormones on distinct systems and also sex differences in evolved behavioral responses that demand different levels of peripheral physiological activation. Studies that examine both subjective reports of negative affect and physiological responses indicate that beginning in adolescence, females respond to acute stressors with more intense negative affect than males despite their comparatively lower peripheral physiological responses. This dissociation is not clearly explained by sex differences in the strength of the relationship between physiological and subjective responses. We suggest that females' greater subjective responsivity may instead arise from a greater activity in brain regions that translate stress responses to subjective awareness in adolescence. Future research directions include investigations of the role of pubertal hormones in physiological reactivity across all systems, examining the relationship of corticolimbic reactivity and negative affect, and sex differences in emotion regulation processes.

    View details for DOI 10.1016/j.psyneuen.2012.01.002

    View details for Web of Science ID 000306583100002

    View details for PubMedID 22281210

  • Developmental changes in brain function underlying the influence of reward processing on inhibitory control. Developmental cognitive neuroscience Padmanabhan, A., Geier, C. F., Ordaz, S. J., Teslovich, T., Luna, B. 2011; 1 (4): 517-529

    View details for DOI 10.1016/j.dcn.2011.06.004

    View details for PubMedID 21966352

  • Effects of response preparation on developmental improvements in inhibitory control ACTA PSYCHOLOGICA Ordaz, S., Davis, S., Luna, B. 2010; 134 (3): 253-263


    Studies in adults indicate that response preparation is crucial to inhibitory control, but it remains unclear whether preparation contributes to improvements in inhibitory control over the course of childhood and adolescence. In order to assess the role of response preparation in developmental improvements in inhibitory control, we parametrically manipulated the duration of the instruction period in an antisaccade (AS) task given to participants from ages 8 to 31 years. Regressions showing a protracted development of AS performance were consistent with existing research, and two novel findings emerged. First, all participants showed improved performance with increased preparation time, indicating that response preparation is crucial to inhibitory control at all stages of development. Preparatory processes did not deteriorate at even the longest preparatory period, indicating that the youngest participants were able to sustain preparation at even the longest interval. Second, developmental trajectories did not differ for different preparatory period lengths, highlighting that the processes supporting response preparation continue to mature in tandem with improvements in AS performance. Our findings suggest that developmental improvements are not simply due to an inhibitory system that is faster to engage but may also reflect qualitative changes in the processes engaged during the preparatory period.

    View details for DOI 10.1016/j.actpsy.2010.02.007

    View details for Web of Science ID 000279660400001

    View details for PubMedID 20347061

  • Are there differences in brain morphometry between twins and unrelated singletons? A pediatric MRI study GENES BRAIN AND BEHAVIOR Ordaz, S. J., Lenroot, R. K., Wallace, G. L., Clasen, L. S., Blumenthal, J. D., Schmitt, J. E., Giedd, J. N. 2010; 9 (3): 288-295


    Twins provide a unique capacity to explore relative genetic and environmental contributions to brain development, but results are applicable to non-twin populations only to the extent that twin and singleton brains are alike. A reason to suspect differences is that as a group twins are more likely than singletons to experience adverse prenatal and perinatal events that may affect brain development. We sought to assess whether this increased risk leads to differences in child or adolescent brain anatomy in twins who do not experience behavioral or neurological sequelae during the perinatal period. Brain MRI scans of 185 healthy pediatric twins (mean age = 11.0, SD = 3.6) were compared to scans of 167 age- and sex-matched unrelated singletons on brain structures measured, which included gray and white matter lobar volumes, ventricular volume, and area of the corpus callosum. There were no significant differences between groups for any structure, despite sufficient power for low type II (i.e. false negative) error. The implications of these results are twofold: (1) within this age range and for these measures, it is appropriate to include healthy twins in studies of typical brain development, and (2) findings regarding heritability of brain structures obtained from twin studies can be generalized to non-twin populations.

    View details for DOI 10.1111/j.1601-183X.2009.00558.x

    View details for Web of Science ID 000276604800004

    View details for PubMedID 20100212

  • A Twin Study of Intracerebral Volumetric Relationships BEHAVIOR GENETICS Schmitt, J. E., Wallace, G. L., Lenroot, R. K., Ordaz, S. E., Greenstein, D., Clasen, L., Kendler, K. S., Neale, M. C., Giedd, J. N. 2010; 40 (2): 114-124


    Using high resolution magnetic resonance imaging data, we examined the interrelationships between eight cerebral lobar volumetric measures via both exploratory and confirmatory factor analyses in a large sample (N = 484) of pediatric twins and singletons. These analyses suggest the presence of strong genetic correlations between cerebral structures, particularly between regions of like tissue type or in spatial proximity. Structural modeling estimated that most of the variance in all structures is associated with highly correlated lobar latent factors, with differences in genetic covariance and heritability driven by a common genetic factor that influenced gray and white matter differently. Reanalysis including total brain volume as a covariate dramatically reduced the total residual variance and disproportionately influenced the additive genetic variance in all regions of interest.

    View details for DOI 10.1007/s10519-010-9332-6

    View details for Web of Science ID 000274964000002

    View details for PubMedID 20112130

  • Variance decomposition of MRI-based covariance maps using genetically informative samples and structural equation modeling NEUROIMAGE Schmitt, J. E., Lenroot, R. K., Ordaz, S. E., Wallace, G. L., Lerch, J. P., Evans, A. C., Prom, E. C., Kendler, K. S., Neale, M. C., Giedd, J. N. 2009; 47 (1): 56-64


    The role of genetics in driving intracortical relationships is an important question that has rarely been studied in humans. In particular, there are no extant high-resolution imaging studies on genetic covariance. In this article, we describe a novel method that combines classical quantitative genetic methodologies for variance decomposition with recently developed semi-multivariate algorithms for high-resolution measurement of phenotypic covariance. Using these tools, we produced correlational maps of genetic and environmental (i.e. nongenetic) relationships between several regions of interest and the cortical surface in a large pediatric sample of 600 twins, siblings, and singletons. These analyses demonstrated high, fairly uniform, statistically significant genetic correlations between the entire cortex and global mean cortical thickness. In agreement with prior reports on phenotypic covariance using similar methods, we found that mean cortical thickness was most strongly correlated with association cortices. However, the present study suggests that genetics plays a large role in global brain patterning of cortical thickness in this manner. Further, using specific gyri with known high heritabilities as seed regions, we found a consistent pattern of high bilateral genetic correlations between structural homologues, with environmental correlations more restricted to the same hemisphere as the seed region, suggesting that interhemispheric covariance is largely genetically mediated. These findings are consistent with the limited existing knowledge on the genetics of cortical variability as well as our prior multivariate studies on cortical gyri.

    View details for DOI 10.1016/j.neuroimage.2008.06.039

    View details for Web of Science ID 000266975300009

    View details for PubMedID 18672072

  • Differences in Genetic and Environmental Influences on the Human Cerebral Cortex Associated With Development During Childhood and Adolescence HUMAN BRAIN MAPPING Lenroot, R. K., Schmitt, J. E., Ordaz, S. J., Wallace, G. L., Neale, M. C., Lerch, J. P., Kendler, K. S., Evans, A. C., Giedd, J. N. 2009; 30 (1): 163-174


    In this report, we present the first regional quantitative analysis of age-related differences in the heritability of cortical thickness using anatomic MRI with a large pediatric sample of twins, twin siblings, and singletons (n = 600, mean age 11.1 years, range 5-19). Regions of primary sensory and motor cortex, which develop earlier, both phylogenetically and ontologically, show relatively greater genetic effects earlier in childhood. Later developing regions within the dorsal prefrontal cortex and temporal lobes conversely show increasingly prominent genetic effects with maturation. The observation that regions associated with complex cognitive processes such as language, tool use, and executive function are more heritable in adolescents than children is consistent with previous studies showing that IQ becomes increasingly heritable with maturity(Plomin et al. 1997: Psychol Sci 8:442-447). These results suggest that both the specific cortical region and the age of the population should be taken into account when using cortical thickness as an intermediate phenotype to link genes, environment, and behavior.

    View details for DOI 10.1002/hbm.20494

    View details for Web of Science ID 000262397000014

    View details for PubMedID 18041741

  • Neurodevelopment and executive function in autism DEVELOPMENT AND PSYCHOPATHOLOGY O'Hearn, K., Asato, M., Ordaz, S., Luna, B. 2008; 20 (4): 1103-1132


    Autism is a neurodevelopmental disorder characterized by social and communication deficits, and repetitive behavior. Studies investigating the integrity of brain systems in autism suggest a wide range of gray and white matter abnormalities that are present early in life and change with development. These abnormalities predominantly affect association areas and undermine functional integration. Executive function, which has a protracted development into adolescence and reflects the integration of complex widely distributed brain function, is also affected in autism. Evidence from studies probing response inhibition and working memory indicate impairments in these core components of executive function, as well as compensatory mechanisms that permit normative function in autism. Studies also demonstrate age-related improvements in executive function from childhood to adolescence in autism, indicating the presence of plasticity and suggesting a prolonged window for effective treatment. Despite developmental gains, mature executive functioning is limited in autism, reflecting abnormalities in wide-spread brain networks that may lead to impaired processing of complex information across all domains.

    View details for DOI 10.1017/S0954579408000527

    View details for Web of Science ID 000260993800005

    View details for PubMedID 18838033

  • Identification of genetically mediated cortical networks: A multivariate study of pediatric twins and siblings CEREBRAL CORTEX Schmitt, J. E., Lenroot, R. K., Wallace, G. L., Ordaz, S., Taylor, K. N., Kabani, N., Greenstein, D., Lerch, J. P., Kendler, K. S., Neale, M. C., Giedd, J. N. 2008; 18 (8): 1737-1747


    Structural magnetic resonance imaging data from 308 twins, 64 singleton siblings of twins, and 228 singletons were analyzed using structural equation modeling and selected multivariate methods to identify genetically mediated intracortical associations. Principal components analyses (PCA) of the genetic correlation matrix indicated a single factor accounting for over 60% of the genetic variability in cortical thickness. When covaried for mean global cortical thickness, PCA, cluster analyses, and graph models identified genetically mediated fronto-parietal and occipital networks. Graph theoretical models suggest that the observed genetically mediated relationships follow small world architectural rules. These findings are largely concordant with other multivariate studies of brain structure and function, the twin literature, and current understanding on the role of genes in cortical neurodevelopment.

    View details for DOI 10.1093/cercor/bhm211

    View details for Web of Science ID 000257787300001

    View details for PubMedID 18234689

  • A multivariate analysis of neuroanatomic relationships in a genetically informative pediatric sample NEUROIMAGE Schmitt, J. E., Wallace, G. L., Rosenthal, M. A., Molloy, E. A., Ordaz, S., Lenroot, R., Clasen, L. S., Blumenthal, J. D., Kendler, K. S., Neale, M. C., Giedd, J. N. 2007; 35 (1): 70-82


    An important component of brain mapping is an understanding of the relationships between neuroanatomic structures, as well as the nature of shared causal factors. Prior twin studies have demonstrated that much of individual differences in human anatomy are caused by genetic differences, but information is limited on whether different structures share common genetic factors. We performed a multivariate statistical genetic analysis on volumetric MRI measures (cerebrum, cerebellum, lateral ventricles, corpus callosum, thalamus, and basal ganglia) from a pediatric sample of 326 twins and 158 singletons. Our results suggest that the great majority of variability in cerebrum, cerebellum, thalamus and basal ganglia is determined by a single genetic factor. Though most (75%) of the variability in corpus callosum was explained by additive genetic effects these were largely independent of other structures. We also observed relatively small but significant environmental effects common to multiple neuroanatomic regions, particularly between thalamus, basal ganglia, and lateral ventricles. These findings are concordant with prior volumetric twin studies and support radial models of brain evolution.

    View details for DOI 10.1016/j.neuroimage.2006.04.232

    View details for Web of Science ID 000244894000008

    View details for PubMedID 17208460

  • A pediatric twin study of brain morphometry JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY Wallace, G. L., Schmitt, J. E., Lenroot, R., Viding, E., Ordaz, S., Rosenthal, M. A., Molloy, E. A., Clasen, L. S., Kendler, K. S., Neale, M. C., Giedd, J. N. 2006; 47 (10): 987-993


    Longitudinal pediatric neuroimaging studies have demonstrated increasing volumes of white matter and regionally-specific inverted U shaped developmental trajectories of gray matter volumes during childhood and adolescence. Studies of monozygotic and dyzygotic twins during this developmental period allow exploration of genetic and non-genetic influences on these developmental trajectories.Magnetic resonance imaging brain scans were acquired on a pediatric sample of 90 monozygotic twin pairs, 38 same-sex dyzygotic twin pairs, and 158 unrelated typically developing singletons. Structural equation modeling was used to estimate the additive genetic, common environment, and unique environment effects, as well as age by heritability interactions, on measures of brain volumes from these images.Consistent with previous adult studies, additive genetic effects accounted for a substantial portion of variability in nearly all brain regions with the notable exception of the cerebellum. Significant age by heritability interactions were observed with gray matter volumes showing a reduction in heritability with increasing age, while white matter volume heritability increased with greater age.Understanding the relative contributions of genetic and nongenetic factors on developmental brain trajectories may have implications for better understanding brain-based disorders and typical cognitive development.

    View details for DOI 10.1111/j.1469-7610.2006.01676.x

    View details for Web of Science ID 000241625200003

    View details for PubMedID 17073977

  • Puberty-related influences on brain development. Molecular and cellular endocrinology Giedd, J. N., Clasen, L. S., Lenroot, R., Greenstein, D., Wallace, G. L., Ordaz, S., Molloy, E. A., Blumenthal, J. D., Tossell, J. W., Stayer, C., Samango-Sprouse, C. A., Shen, D., Davatzikos, C., Merke, D., Chrousos, G. P. 2006; 254-255: 154-162


    Puberty is a time of striking changes in cognition and behavior. To indirectly assess the effects of puberty-related influences on the underlying neuroanatomy of these behavioral changes we will review and synthesize neuroimaging data from typically developing children and adolescents and from those with anomalous hormone or sex chromosome profiles. The trajectories (size by age) of brain morphometry differ between boys and girls, with girls generally reaching peak gray matter thickness 1-2 years earlier than boys. Both boys and girls with congenital adrenal hyperplasia (characterized by high levels of intrauterine testosterone), have smaller amygdala volume but the brain morphometry of girls with CAH did not otherwise significantly differ from controls. Subjects with XXY have gray matter reductions in the insula, temporal gyri, amygdala, hippocampus, and cingulate-areas consistent with the language-based learning difficulties common in this group.

    View details for PubMedID 16765510

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