Ahmad R. Hariri - US grants
Affiliations: | University of Pittsburgh, Pittsburgh, PA, United States |
Area:
fMRI, Genetics, Emotion, SerotoninWe are testing a new system for linking grants to scientists.
The funding information displayed below comes from the NIH Research Portfolio Online Reporting Tools and the NSF Award Database.The grant data on this page is limited to grants awarded in the United States and is thus partial. It can nonetheless be used to understand how funding patterns influence mentorship networks and vice-versa, which has deep implications on how research is done.
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High-probability grants
According to our matching algorithm, Ahmad R. Hariri is the likely recipient of the following grants.| Years | Recipients | Code | Title / Keywords | Matching score |
|---|---|---|---|---|
| 2005 — 2009 | Hariri, Ahmad R | K01Activity Code Description: For support of a scientist, committed to research, in need of both advanced research training and additional experience. |
Development of Amygdala-Prefrontal Interactions @ University of Pittsburgh At Pittsburgh DESCRIPTION (provided by applicant): This revised application for a Mentored Research Scientist Development Award (RFA-PA-95-049 K01) describes a career development and research plan with a long-term goal of understanding the neural bases of affect dysregulation (and affective disorders) in adolescence. The approach build's upon the applicant's previous neuroimaging studies of genetic influences on the functional dynamics of the amygdala and prefrontal cortex in adults. This application seeks to extend that line of investigation into a specific developmental and clinical framework to address key questions about affect regulation and pubertal brain maturation relevant for adolescent affective disorders. The training plan emphasizes a cognitive and affective neuroscience approach to understanding the development of affect regulation; it also includes specific activities aimed at increasing the applicant's knowledge of developmental, clinical, statistical and ethical issues relevant to this line of investigation. The research plan builds upon a well-established program project investigating neurobehavioral changes in pediatric affective disorders (P01-MH41712). Component one of the research plan involves the addition of genotyping and a neuroimaging study to an existing protocol that includes samples of depressed, anxiety disordered, and normal control children and adolescents. Component two involves the recruitment of a new sample of female controls to address a specific question about the impact of the pubertal rise in estrogen on amygdala-prefrontal functional interactions in normal development. Together, these studies and training program will enable the applicant to advance understanding of genetic and maturational influences on the development of affect regulation during adolescence within an affective neuroscience framework in ways that will help inform the etiology and diathesis (and eventually, more effective treatment) of early onset affective disorders. |
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| 2010 — 2012 | Hariri, Ahmad R Strauman, Timothy J [⬀] |
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. |
Self-Regulation Failure: Identifying and Modifying a Risk Phenotype @ Duke University DESCRIPTION (provided by applicant): Human behavior involves the unique capacities to regulate our own psychological states to pursue desired goals, bring our behavior in line with internal/external standards, manage our emotions, and cope with challenges and opportunities that arise. The term self-regulation denotes the processes through which people intentionally or automatically initiate, maintain, and terminate their own thoughts and behaviors in the service of pursuing personal goals. The importance of understanding self-regulation becomes obvious when one considers the array of public health problems that can be traced to problematic goal pursuit. Many behaviors that put people at increased risk for illness, disability, and death - such as obesity, eating disorders, smoking, alcohol abuse, suicidality, and drug addiction - involve difficulties with self-regulation. Thus, maladaptive self-regulation is an important contributory factor in a large number of psychological, social, and health-related problems. We believe that significant progress can be made in understanding and overcoming self- regulatory problems by combining existing theory and research in behavioral science with parallel findings in related disciplines. Recent developments in cognitive neuroscience (specifically, the role of the orbitofrontal cortex in self-regulation of goal pursuit) and imaging genetics (specifically, how heritable variability in the gene encoding catechol-O- methyltransferase [COMT], an enzyme that controls extracellular dopamine in the frontal cortex, influences processing of motivationally salient stimuli) offer synergistic perspectives on how failure in self-regulation could, for a particular subset of individuals, lead to chronically maladaptive behavior and increase vulnerability to a range of significant health problems. The aims of this R01 application are: (1) to validate a hypothesized gene/environment/self-regulation risk phenotype conferring vulnerability to failures of self- regulation, and (2) to test a novel set of cognitive/behavioral techniques that we predict will acutely reverse the dysfunctions that underlie self-regulatory failure. The proposed research will be conducted in two samples: adolescents, who are vulnerable to initiation of a number of health-risking behaviors and psychological problems, and college students, some of whom already engage regularly in such behaviors and manifest psychological difficulties. We predict that a combination of three contributory factors - individual differences in regulatory focus, COMT genotype, and chronic failure to attain a particular kind of personal goal - creates a self- regulation pathway to disordered behaviors with significant public health implications. PUBLIC HEALTH RELEVANCE: The aims of this R01 application are: (1) to conduct a program of translational research validating a hypothesized gene/environment/self-regulation risk phenotype conferring vulnerability to failures of self-regulation, and (2) to test a novel set of cognitive/behavioral techniques that we predict will acutely reverse the dysfunctions that underlie self-regulatory failure. We predict that we will observe, in both adolescent and college student samples, that a combination of three contributory factors - individual differences in regulatory focus, COMT genotype, and chronic failure to attain a particular kind of personal goal - creates a self- regulation pathway to a broad array of disordered behaviors and psychological states with significant public health implications, including tobacco use, alcoholism, mood disorders, obesity, eating disorders, and impulsivity. Based on this model, we anticipate that the theory- based brief change techniques will prove efficacious and will ultimately provide a basis for effective broader-scale therapeutic and preventive interventions in future studies. |
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| 2013 — 2016 | Hariri, Ahmad R | 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. |
Neurogenetic Pathways to Drug Use in Young Adults @ Duke University DESCRIPTION (provided by applicant): The primary aim of the current application is to test a novel model of how the relative responsiveness of reward- and threat-related neural circuits interact with life stress to predict drug use in a large cohort of adolescents and young adults. The application also aims to identify genetic profiles representing variability in key neuromodulatory pathways that predict these interactions. To address these specific aims the application will collect measures of: 1) core behavioral processes that serve as risk factors for drug use and abuse, 2) brain circuits supporting threat and reward responsiveness as well as behavioral control, 3) the experience of stressful life events and 4) DNA sequence variation in 600 18-22 year old undergraduates. All measures will be collected using the existing extensive research infrastructure of the Duke Neurogenetics Study. Innovative analytic strategies for modeling individual differences will be applied to these data in the service of identifying behavioral, neurobiological, environmental and genetic mechanisms mediating variability in risk behaviors. The predictive utility of our findings for informing developmental trajectories of drug use, abuse, and dependence will be tested through federated studies. These studies are collecting overlapping measures in both community samples as well as longitudinal samples of patients and individuals at high risk (e.g., low SES, positive family history). Data federation wil also provide replication data sets and/or additional power for testing novel associations between neural, genetic, and environmental variation and the emergence of psychopathology. Furthermore, existing collaborations with investigators using animal models of human behavior and disease as well as those conducting epidemiological gene-environment interaction research will facilitate unique translational projects based on our findings. These collaborations will allo for identification of both detailed molecular mechanisms and broader clinical relevance. Collectively, the research proposed will reveal mechanisms and pathways that predict psychopathology with a focus on drug use and the transition to abuse, which represents a major thrust of current research supported by NIDA and is consistent with the Research Domain Criteria (RDoC) emphasis on classifying psychopathology based on dimensions of observable behavior and neurobiological measures. |
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| 2014 | Hariri, Ahmad R Suglia, Shakira Franco |
R21Activity Code Description: To encourage the development of new research activities in categorical program areas. (Support generally is restricted in level of support and in time.) |
Epigenetic Links Between the Social Environment and Emotional Brain Function @ Columbia University Health Sciences DESCRIPTION (provided by applicant): This application is submitted in response to RFA-TW-13-002. The broad goal of this application is to collect pilot data for an R01 application aimed at identifying functionally relevant DNA methylation (DNAm) signatures in saliva that mediate the relation between the social environment and individual differences in behaviorally and clinically relevant neural phenotypes. This application will build on the unique resource of the Duke Neurogenetics Study (DNS). The DNS seeks to advance our understanding of biological mechanisms and pathways predicting variability in behaviors associated with risk for psychopathology. This broad aim is achieved through the systematic measurement and integration of genes, brain, environment, and behavior in 18-22 year old young adults. Behavioral, clinical, experiential, neuroimaging, and DNA data are already available for 207 DNS participants, and these data are ready for the analyses detailed in this application. Moreover, the DNS is funded by NIDA to continue data collection through February 28. 2017, which will provide approximately 200 additional samples for methylation assays under this application. Through hypothesis-driven analysis of continuous measures of brain function through neuroimaging and common variation in the genome, this research both recognizes the growing importance of dimensional phenotypes as described in the NIMH RDoC, and provides a foundation from which to examine how specific social environmental risks influence neurogenetic trajectories of relative risk and resilience that will inform ongoing efforts to advance treatment and prevention of mental illness. Evidence suggests DNAm is reversible, and therefore, this work will provide insights into why and how changing social environments are associated with rapid changes in behavior and clinically-relevant outcomes and, conversely, how we might influence the impact of adverse social environments on human health. The proposed methylation assays on the existing and planned DNA samples will allow us to address the following aims: 1) Using salivary DNA, to identify DNAm signatures in coding regions of candidate genes associated with functional neural phenotypes (e.g. threat related amygdala reactivity) related to psychopathology; 2) To examine whether social stressors are associated with DNAm signatures identified in Aim 1, and whether DNAm signatures explain the relation between social environment and functional neural phenotypes. Our work will contribute directly to the mission of RFA-TW-13-002, by revealing potential pathways for how modifiable social exposure(s) that act through epigenetic processes produce changes in brain function known to be behaviorally and clinically relevant. The identification of reliable DNAm signatures in saliva that are correlated with brain function would be, in itself, a huge advance for the field. This pilt study will lay the groundwork for longitudinal work to test the directionality of observed associations and for in vitro work aimed at determining how DNAm signatures observed here are translated into observable differences in neural phenotypes. |
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| 2015 — 2019 | Hariri, Ahmad R Moffitt, Terrie E (co-PI) [⬀] |
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. |
Neural Signatures of Healthy and Unhealthy Aging @ Duke University ? DESCRIPTION (provided by applicant): Declining fertility rates, aging of the baby-boomers, and increasing life expectancy are leading to population aging. As the population ages, this increases the public-health impact of age-related conditions, such as cardiovascular disease, type 2 diabetes, and dementia. Treating un-prevented diseases in late life has proven costly and ineffective. Consequently, effective strategies are needed in midlife to prevent age-related diseases and to improve the quality of longer lives. It is now known that potentially preventable risk exposures and physiological causes of age-related disease emerge in childhood. This recognition lends new scientific significance to studies that have followed cohorts from childhood. It is also now known that the pathogenesis of age-related diseases involves gradually accumulating damage to organ systems, beginning in the first half of the life course. Of these organ systems, the central nervous system is integral, prompting our proposal to add neuroimaging to the Dunedin Multidisciplinary Health & Development Study, a longitudinal study of both problematic and positive processes of adult development and aging, in a birth cohort now entering its fifth decade. This study combines methods of demographic/economic surveys, clinical-quality health assessments, biobanking, and linkage to nationwide administrative records (health, welfare, finances). We propose to administer a multimodal MRI protocol to the 1004 living members of the birth cohort. Our proposed neuroimaging protocol will measure individual variation in brain function, structure, and connectivity. We focus on the hubs of four neural circuits and the core behavioral capacities each supports: (1) the amygdala and emotion/threat, (2) the ventral striatum and motivation/reward, (3) the hippocampus and memory, and (4) the dorsolateral prefrontal cortex and executive control. With the resulting midlife neural measures, we propose three primary aims that will generate findings about problematic and successful aging: Aim 1 tests whether prospectively ascertained early- life adversity is linked to midlife neural measures. Aim 2 tests whether neural measures are linked to real-world behaviors (e.g., saving behavior) necessary to prepare for successful aging. Aim 3 tests if neural measures are related to the accelerated pace of biological aging. The proposed work will improve knowledge by generating findings about the neural correlates of age-related diseases and successful healthy aging. These findings are expected to support preventing disease and enhancing preparedness for wellbeing in late life. Beyond the proposed 5-year project, follow-up neuroimaging is envisaged. This project thus brings neuroimaging into three timely and vigorous areas of aging science: the study of early-life programming of lifelong health, the study of midlife preparation for successful aging, and mind-body research linking brain function to physical health. |
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