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High-probability grants
According to our matching algorithm, Katie A. McLaughlin is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2014 — 2017 |
Mclaughlin, Katie |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Child Trauma and the Development of Neural Systems Underlying Emotion Regulation @ University of Washington
DESCRIPTION (provided by applicant): Childhood trauma exposure is strongly associated with psychopathology onset in children, adolescents, and adults, accounting for a substantial proportion of mental disorders in the population. However, the neurodevelopmental mechanisms that explain the association between child trauma (CT) and psychopathology remain poorly characterized. In particular, research examining how CT influences brain development remains in its infancy. Yet understanding the neurodevelopmental processes that are disrupted as a result of CT exposure will provide critical information about the pathways linking adverse environments to psychopathology. To that end, the proposed project examines the impact of CT on the development of neural networks involved in emotion regulation, a plausible neurobiological pathway linking CT to psychopathology. The proposed research addresses Objective 1 of the NIMH Strategic Plan by examining how specific types of early environmental experience-child physical or sexual abuse and domestic violence-alter neural structure and function in ways that might increase risk for psychopathology. We hypothesize that CT exposure disrupts the development of the prefrontal cortex (PFC) and amygdala, resulting in atypical patterns of neural function and reduced structural and functional connectivity between these regions. We aim to build knowledge of how environmental experience shapes development in Negative Valence Systems by applying a neurobiological model distinguishing between emotional reactivity and both implicit and explicit emotion regulation to investigate this hypothesis. Specifically, we propose that a) CT exposure leads to heightened amygdala reactivity and that reactivity is positively associated with trauma severity and chronicity, and b) chronicity of exposure to CT is additionally associated with deficits in emotion regulation, involving poor PFC modulation of amygdala reactivity resulting from low structural and functional connectivity between these regions. The conceptual model will be tested by acquiring structural and functional MRI data in a sample of 8- 16 year olds; half with exposure to child maltreatment or domestic violence and half without exposure to CT or interpersonal violence. The sample will be recruited to ensure variation in CT chronicity and severity and to allow us to examine associations of CT with neural structure and function in children with and without pre- existing internalizing psychopathology. The proposed study builds on existing research examining the influence of early deprivation on brain development by examining how experiences of threat influence neural structure and function in children. Study findings will provide critical information regarding the specific aspects of emotional reactivity ad regulation that are disrupted following CT exposure. Elucidating these mechanisms will not only build knowledge of how adverse environments alter neural development in ways that might increase risk for psychopathology, but will also suggest possible targets for preventive interventions aimed at reducing psychopathology risk in children exposed to trauma.
|
0.915 |
2016 — 2020 |
Mclaughlin, Katie |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Deprivation and Threat: Dimensions of Early Experience and Neural Development @ University of Washington
? DESCRIPTION (provided by applicant): Extensive research finds robust links between mental health and childhood adversity (CA), encompassing diverse exposures from child abuse to poverty. Despite the strength and consistency of these findings, the mechanisms producing such links remain poorly specified. In particular, past research has failed to identify how specifi environmental experiences influence specific neural processes. Such limitations arise from the difficulty of precisely quantifying relevant CA and neural variables in children. The current proposal addresses these limitations by capitalizing on a unique, well characterized NIH-funded longitudinal cohort of children where multiple aspects of CA have been precisely assessed and use of rigorous neuroimaging methods to quantify functioning in specific neural circuits. We will use these methods to test a novel conceptual framework delineating how specific types of environmental experience influence specific neural processes, addressing Objective 1 of the NIMH Strategic Plan. Our model argues that different types of CA have distinct effects on neural development. The central distinction we make is between trauma and deprivation. Trauma exposure involves harm or threat of harm, resulting in fear learning mediated by limbic pathways that are well characterized in animals and conserved across species. We argue that child trauma alters development of circuits in the Negative Valence System that support emotional learning encompassing amygdala and ventromedial prefrontal cortex (PFC). In contrast, deprivation involves absence of expected cognitive and social inputs and environmental complexity. Animal research shows that deprivation disrupts development in PFC and parietal cortex by hijacking the typical process of synaptic pruning. Thus we predict that social-cognitive deprivation influences Cognitive Control Systems, resulting in age-specific reductions in thickness and volume of dorsolateral PFC and superior parietal cortex and reduced performance on cognitive control tasks supported by these areas. Clearly, trauma and deprivation are correlated. Our unique design will measure these experiences on separate dimensions informed by rich preliminary data indicating distinct effects of trauma and deprivation on neural development even in samples with high exposure co-occurrence. Our proposed conceptual model will be tested by acquiring structural and functional MRI data on an existing sample of 300 children (1/3 in poverty, 1/3 near poverty, and 1/3 middle class) followed since early childhood with significant variability in CA exposure. Psychopathology has been measured in previous waves of the study and will be collected multiple times during the study period. Study findings will provide critical information about how specific dimensions of environmental experience influence specific neural processes. Elucidating these mechanisms will not only build knowledge of how adverse environments alter neural development in ways that increase risk for psychopathology, but will also suggest possible targets for preventive interventions aimed at reducing psychopathology risk in children exposed to trauma and deprivation.
|
0.915 |