Michael C Stevens
Hartford Hospital
Project start date: 2009-04-17
Project end date: 2014-01-31
Sponsored Links Excellgen http://Excellgen.com
ADOLESCENT MATURATION OF BRAIN NETWORK INTEGRATION FOR EXECUTIVE CONTROL ABILITIE
Michael C Stevens, Director, Clinical Neurosci & Developmen
Hartford Hospital, Hartford, Ct 06102
Grant 5R01MH081969-02 from National Institute Of Mental Health
Abstract: Adolescence is a distinct developmental period during which
Keywords: neural constructivism, ` which predicts that ongoing refinement of cognitive abilities present by puberty is accomplished largely by experience-dependent changes in how brain regions participate in functionally-defined networks. Although many previous neuroimaging studies have found age-related changes in brain structure and activity levels that are consistent with neural constructivist theory predictions, there has been no direct test of this hypothesis. Specifically, no study has directly examined functional connectivity changes with age to confirm increasing integration of task-engaged brain regions throughout adolescence. Moreover, the relationship between brain activity and executive test performance changes during typical adolescent development is virtually unexamined.
Relevance: executive´ control over behavior and cognition improves towards mature, adult levels of performance on neuropsychological tests. It has been proposed that these cognitive gains are the product of increasing neural specialization and functional integration of numerous functionally-specialized brain regions that are engaged for task performance. This idea is often termed
Project start date: 2009-04-17
Project end date: 2014-01-31
Budget start date: 1-FEB-2010
Budget end date: 31-JAN-2011
PFA/PA: CHARACTERIZING TWO DISTINCT ADHD NEUROBIOLOGIES WITH FMRI
Michael C Stevens, Director, Clinical Neurosci & Developmen
Hartford Hospital, Hartford, Ct 06102
Grant 5R01MH080956-03 from National Institute Of Mental Health
Abstract: This project will use functional magnetic resonance imaging (fMRI) to characterize dysfunction in two theoretically separable neurocognitive pathways in adolescents with Attention-Deficit/Hyperactivity Disorder (ADHD). ADHD is a common disorder arising in childhood that often results in lifelong educational, social, and occupational impairment. Decades of research has greatly refined our appreciation of the disorder´s complexity. To date, no study has managed to identify an effective biological marker, a single neuropsychological test, or a specific genetic profile that accurately identifies persons with ADHD, in part because previous studies have produced inconsistent findings. Many researchers have concluded that this is because the etiology of ADHD is multi-factorial, probably polygenetic in nature, involving numerous small influences on brain function. Consistent evidence points to a hypodopaminergic state in frontostriatal brain regions, hypothesized to result in at least two forms of neurocognitive impairment linked to impulsive ADHD symptoms impaired
Relevance: executive´ performance on tests requiring inhibition of response, and impaired motivation measured by tests assessing insensitivity to delayed reinforcement. Although this model is supported by neuropsychological evidence, functional neuroimaging studies have not yet fully characterized the biological pathology giving rise to these cognitive deficits. It is likely that much of the inconsistency in previous ADHD neurocognitive research results from examining samples with heterogeneous pathologies. Understanding the major sources of neurobiological heterogeneity is the most significant step in future research of ADHD, and ultimately will help clinicians better diagnose and treat the disorder. This project seeks to characterize the functional neuroanatomy of these two ADHD neurocognitive impairments by examining the association of neuropsychological profile, mesocortical and mesolimbic brain dysfunction, and candidate gene susceptibilities. Participants will be 130 adolescents diagnosed with Combined-subtype ADHD (DSM 314.01) and 130 demographically-matched healthy controls. All participants will undergo rigorous psychiatric evaluation, neuropsychological assessment of several different cognitive domains, fMRI measurement of response inhibition and reward system brain activity, and genotyping DAT1, DRD4, plus several other dopamine-related genetic markers previously linked to ADHD. These data will allow us to validate the presence of two separate brain function pathologies in ADHD and to clarify relationships among disordered brain function, cognitive performance and genotype. The planned project is highly collaborative between experts in functional neuroimaging, cognitive testing, clinical assessment and psychiatric genetics. The neurobiological basis of Attention-Deficit/Hyperactivity Disorder is poorly understood because a single reliable biomarker or definitive test for the disorder has yet to be identified. There is evidence from cognitive studies of ADHD youth that impulsive behavior may arise from two markedly different types of neurobiological dysfunction. This project will use functional magnetic resonance imaging (fMRI) to link these two profiles of abnormal brain function in ADHD adolescents to specific types of neuropsychological dysfunction and to certain genetic markers, providing support for the clinical use of these tools to more precisely diagnose biologically-meaningful subtypes of ADHD. The neurobiological basis of Attention-Deficit/Hyperactivity Disorder is poorly understood because a single reliable biomarker or definitive test for the disorder has yet to be identified. There is evidence from cognitive studies of ADHD youth that impulsive behavior may arise from two markedly different types of neurobiological dysfunction. This project will use functional magnetic resonance imaging (fMRI) to link these two profiles of abnormal brain function in ADHD adolescents to specific types of neuropsychological dysfunction and to certain genetic markers, providing support for the clinical use of these tools to more precisely diagnose biologically-meaningful subtypes of ADHD
Project start date: 2008-05-15
Project end date: 2013-03-31
Budget start date: 1-APR-2010
Budget end date: 31-MAR-2011
PFA/PA: AN FMRI STUDY OF THE EFFECT OF WORKING MEMORY TRAINING ON ADHD BRAIN DYSFUNCTION
Michael C Stevens
Hartford Hospital, Hartford, Ct 06102
Grant 1R21HD061915-01A1 from Eunice Kennedy Shriver National Institute Of Child Health & Human Development
Abstract: There is evidence both that computer-administered cognitive training can improve ADHD working memory deficits and that this type of training in non-ADHD enhances normal working memory ability by altering brain activity in prefrontal cortex and the parietal lobe. However, no study has characterized brain activity changes following working memory training in ADHD to understand what neural changes occur when cognitive deficits are remedied. This R21 exploratory study will examine the neural basis of cognitive training treatment gains in working memory, ADHD symptoms, and various other executive abilities. The study will compare n=21 ADHD adolescents with evidence for baseline deficits in working memory (i.e., <1.5 SD below normative ratings at baseline) and n=21 demographically-matched non-ADHD healthy control participants. Participants will undergo baseline neuropsychological and fMRI imaging with verbal and visuospatial Sternberg fMRI working memory tasks, 5 weeks of daily computerized working memory training, and then endpoint fMRI and cognitive evaluation of neural and behavioral changes. Training will utilize commercially-available Cogmed software (www.cogmed.com) as it has a well-developed set of computerized tools, with numerous practical advantages for this study. Our analyses will identify which brain regions in ADHD adolescents are affected by working memory treatment and characterize patterns of activation change between baseline and endpoint. We will examine post-treatment differences in the extent of activation and functional connectivity among activated brain regions to test hypotheses about possible neural mechanisms underlying treatment gains. These analyses will provide data that will permit us to confirm a neurobiological model of the treatment mechanism to permit future studies of this intervention´s effectiveness in ADHD. We also will conduct a series of analyses to determine what specific changes in brain function might underlie a generalized effect of working memory training on ADHD symptoms and other ´executive´ abilities. By identifying the neural correlates any such effect, this study could yield invaluable information about what the neural targets of any effective ADHD treatment must be. The key accomplishment of this exploratory study will be to characterize the neural basis of treatment gains in ADHD by testing theoretically-guided hypotheses about possible neuroplastic changes. The results will support larger, future studies aimed at better understanding the neural basis of this alternative treatment for ADHD, identifying biological or genetic factors that might denote the presence of a remediable working memory deficit, and ultimately achieving a better understanding of the etiology of ADHD working memory deficits. There is evidence both that computer-administered cognitive training can improve ADHD working memory deficits and that this type of training in non-ADHD enhances normal working memory ability by altering brain activity in prefrontal cortex and the parietal lobe. However, no study has characterized brain activity changes following working memory training in ADHD to understand what neural changes occur when cognitive deficits are remedied. This R21 exploratory study will examine the neural basis of cognitive training treatment gains in working memory, ADHD symptoms, and various other executive abilities
Keywords: AD/HD; ADHD; Active Follow-up; Adolescent; Adolescent Youth; Affect; After Care; After-Treatment; Aftercare; Attention deficit hyperactivity disorder; Attention-Deficit Disorder, Predominantly Hyperactive-Impulsive Type; Behavioral; Behavioral Symptoms; Biological; Biological Neural Networks; Brain; Brain region; Causality; Clinical; Cognitive; Cognitive deficits; Communication; Computer Programs; Computer software; Computers; DSM-IV; DSM4; Data; Diagnostic and Statistical Manual of Mental Disorders, 4th edition; Diagnostic and Statistical Manual of Mental Disorders-IV; Disease remission; Dysfunction; Education for Intervention; Educational Intervention; Effectiveness of Interventions; Encephalon; Encephalons; Etiology; Evaluation; Functional Magnetic Resonance Imaging; Functional disorder; Future; Genetic; Hyperactivity Disorder NOS; Hyperactivity Disorder, Predominantly Hyperactive-Impulsive Type; Hyperkinetic Syndrome; Image; Impairment; Instruction Intervention; Intervention Studies; Learning; MRI, Functional; Magnetic Resonance Imaging, Functional; Maintenance; Maintenances; Memory Deficit; Memory impairment; Memory, Immediate; Memory, Short-Term; Memory, Shortterm; Modeling; Nerve Cells; Nerve Unit; Nervous; Nervous System, Brain; Neural Cell; Neurobiology; Neurocyte; Neurons; Outcome; Parietal; Parietal Lobe; Parietal Lobe of the Brain; Participant; Pattern; Performance; Persons; Phase; Physiopathology; Prefrontal Cortex; Process; RMSN; Recruitment Activity; Reliance; Remission; Retrieval; Series; Short-Term Memory; Software; Symptoms; Testing; Training; Training Intervention; Visuospatial; alternative treatment; attention deficit hyperactive disorder; base; cognitive training; computational tools; computer program/software; computerized; computerized tools; disease causation; disease etiology; disease/disorder etiology; disorder etiology; effect of intervention; fMRI; follow-up; functional gain; functional outcomes; imaging; improved; instructional intervention; juvenile; juvenile human; neural; neural mechanism; neural network; neurobiological; neuromechanism; neuronal; neuropsychological; parietal cortex; pathophysiology; public health relevance; recruit; relating to nervous system; visual spatial; working memory
Relevance: There is evidence both that computer-administered cognitive training can improve ADHD working memory deficits and that this type of training in non-ADHD enhances normal working memory ability by altering brain activity in prefrontal cortex and the parietal lobe. However, no study has characterized brain activity changes following working memory training in ADHD to understand what neural changes occur when cognitive deficits are remedied. This R21 exploratory study will examine the neural basis of cognitive training treatment gains in working memory, ADHD symptoms, and various other executive abilities
Project start date: 2010-09-24
Project end date: 2011-08-31
Budget start date: 24-SEP-2010
Budget end date: 31-AUG-2011
PFA/PA: PA-09-164
1R21HD061915-01A1 (2010): $257310
NEUROIMAGING COGNITION IN ADOLESCENT BEHAVIOR DISORDERS
Michael C Stevens, Director, Clinical Neurosci & Developmen
Hartford Hospital, Hartford, Ct 06102
Grant 5K23MH070036-05 from National Institute Of Mental Health
Abstract: Over a 5-year period, I will receive training in event-related potential electroencephalography (ERP EEG), event-related functional magnetic resonance imaging (ER-fMRI), and neuropsychological research techniques with adolescents who have disruptive behavior disorders (DBDs). The purpose of this research is to identify and characterize neurocognitive correlates of traits and behaviors that comprise commonly used classification systems for juvenile DBDs. These training experiences will prepare me to implement a pilot study of DBD brain function in 125 adolescents over the RCA period. It will include functional brain imaging using ERP and ER-fMRI versions of several different tasks designed for sensitivity to neural dysfunction unique to each DBD diagnoses. Previous studies have poorly controlled for the common comorbidity seen in DBD subjects; have incorporated all the recruitment resources and the brain imaging techniques proposed in this project. These data will isolate abnormally functioning neural circuits underlying cognitive abnormalities in antisocial adolescents, compare DBD groups and/or symptom types, and determine associations of these findings to behavioral and neuropsychological measures commonly used in clinical assessment. Through the process of training and pilot research, I will develop (1) expertise in collection, analysis, and interpretation of ERPs and ER-fMRI; (2) expertise in neuropsychological evaluation of antisocial adolescents using developmentally-appropriate measures; and (3) expertise in theories of cognitive dysfunction in DBDs, including what specific mechanisms may underlie symptoms or affect the course of cognitive development of antisocial children into adulthood. With this training and the collection of pilot data I hope to develop an empirically based conceptual framework and the necessary methodological skills to preliminarily address several questions related to juvenile antisocial disorders, including What neural dysfunction is specific to each adolescent DBD diagnosis? What relationship do DBD adolescents´ EEG and ER-fMRI-measured brain activity have with behavioral profile or neuropsychological test results? How do findings compare with neuroimaging results from previous studies of antisocial groups? The overall aim of this project is to prepare me to conduct subsequent prospective studies of DBD adolescents to study changes in neurocognition from adolescence to adulthood using R01 funding mechanisms
Keywords: 0-11 years old; 12-20 years old; 21+ years old; AD/HD; ADHD; Address; Adolescence; Adolescent; Adolescent Behavior; Adolescent Youth; Adult; Affect; Affective; Amygdala; Amygdaloid Body; Amygdaloid Nucleus; Amygdaloid structure; Anterior; Area; Attention deficit hyperactivity disorder; Attention-Deficit Disorder, Predominantly Hyperactive-Impulsive Type; Basal Ganglia; Basal Nuclei; Behavior; Behavior Disorder, Disruptive; Behavior Disorders; Behavioral; Behavioral Symptoms; Bilateral; Biological; Bone callus; Bony Callus; Brain; Brain imaging; Callus; Cerebellum; Child; Child Youth; Children (0-21); Classification; Clinical assessments; Cognition; Cognitive; Cognitive Disturbance; Cognitive Impairment; Cognitive decline; Cognitive deficits; Cognitive function abnormal; Collection; Comorbidity; Conduct Disorder; Corpus Striatum; Corpus striatum structure; DSM-IV; DSM4; Data; Detection; Development; Diagnosis; Diagnostic; Diagnostic and Statistical Manual of Mental Disorders, 4th edition; Diagnostic and Statistical Manual of Mental Disorders-IV; Disease; Disinhibition; Disorder; Disruptive Behavior Disorder; Disturbance in cognition; Dysfunction; EEG; Electrodes; Electroencephalography; Elements; Emotional; Encephalon; Encephalons; Evaluation; Event; Event-Related Potentials; Functional Magnetic Resonance Imaging; Functional disorder; Funding Mechanisms; Human, Adult; Human, Child; Hyperactivity Disorder NOS; Hyperactivity Disorder, Predominantly Hyperactive-Impulsive Type; Hyperkinetic Syndrome; IQ Deficit; Imaging Procedures; Imaging Techniques; Impaired cognition; Impairment; Inferior; Influentials; Investigators; Lateral; Left; MRI, Functional; Magnetic Resonance Imaging, Functional; Measures; Monitor; Morbidity; Morbidity - disease rate; Motor; Msec; Nervous; Nervous System, Brain; Neurobiology; Neurocognition; Neurocognitive; Neurocognitive Deficit; Neurophysiology - biologic function; Neuropsychologic Tests; Neuropsychological Tests; Pattern; Performance; Physiopathology; Pilot Projects; Prefrontal Cortex; Process; Programs (PT); Programs [Publication Type]; Prospective Studies; Purpose; R01 Mechanism; R01 Program; RPG; Relative; Relative (related person); Research; Research Grants; Research Personnel; Research Project Grants; Research Projects; Research Projects, R-Series; Research Resources; Research Technics; Researchers; Resources; Risk; Site; Social Environment; Striate Body; Striatum; Superior temporal gyrus; Symptoms; System; System, LOINC Axis 4; Systematics; Technics, Imaging; Techniques, Research; Test Result; Time; Training; adolescence (12-20); adult human (21+); amygdaloid nuclear complex; anti social; antisocial; attention deficit hyperactive disorder; auditory stimulus; base; behavior disorder diagnosis; behavioral disinhibition; behavioral disorder; brain visualization; children; cognitive dysfunction; cognitive loss; cognitively impaired; design; designing; disease control; disease/disorder; disorder control; disruptive behavioral disorder; event related potential; experience; fMRI; hemodynamics; indexing; juvenile; juvenile human; lexical; millisecond; neural; neural circuit; neural circuitry; neural function; neurobiological; neuroimaging; neuropsychological; pathophysiology; pilot study; programs; psychopathic personality; psychopathy; relating to nervous system; response; skills; social climate; social context; socioenvironment; stem; stimulus processing; striatal; teenage; theories; trait; youngster
Project start date: 2004-08-01
Project end date: 2010-07-31
Budget start date: 1-AUG-2008
Budget end date: 31-JUL-2010
PFA/PA: PA-00-004
5K23MH070036-05 (2008): $0
5K23MH070036-04 (2007): $162868
5K23MH070036-03 (2006): $159697
5K23MH070036-02 (2005): $156619
1K23MH070036-01A1 (2004): $153390
ADOLESCENT MATURATION OF BRAIN NETWORK INTEGRATION FOR EXECUTIVE CONTROL ABILITIE
Michael C Stevens, Director, Clinical Neurosci & Developmen
Hartford Hospital, Hartford, Ct 06102
Grant 3R01MH081969-01A2S1 from National Institute Of Mental Health
Abstract: Adolescence is a distinct developmental period during which ´executive´ control over behavior and cognition improves towards mature, adult levels of performance on neuropsychological tests. It has been proposed that these cognitive gains are the product of increasing neural specialization and functional integration of numerous functionally-specialized brain regions that are engaged for task performance. This idea is often termed ´neural constructivism,´ which predicts that ongoing refinement of cognitive abilities present by puberty is accomplished largely by experience-dependent changes in how brain regions participate in functionally-defined networks. Although many previous neuroimaging studies have found age-related changes in brain structure and activity levels that are consistent with neural constructivist theory predictions, there has been no direct test of this hypothesis. Specifically, no study has directly examined functional connectivity changes with age to confirm increasing integration of task-engaged brain regions throughout adolescence. Moreover, the relationship between brain activity and executive test performance changes during typical adolescent development is virtually unexamined. ´Generative´ models of brain system function emphasize the importance of efficient inter-regional connectivity and network interaction for optimal cognitive function. These models are based on compelling evidence that brain systems are hierarchically-organized, such that ´higher-order´ systems (which include historically-recognized frontal lobe executive brain regions) exert top-down control over subordinate neural systems. This neural model is consistent with the putative organization of executive cognitive abilities, which are commonly proposed to consist of a higher-order cognitive functions that supervise or otherwise influence subsidiary cognitive operations. However, because the study of brain functional connectivity is in its infancy, the probable correspondence between supposed ´top down´ neural system influence and higher-order executive cognition has never been explored. This is a competitive revision submitted for a recently funded R01 to study these topics. We will conduct a 5-year, cross-sectional study (n=130) of normal adolescent to young adult development (ages 12-24). The parent project will examine age-related changes in functional integration and hierarchical top-down influence underlying three behaviorally-dissociable types of executive ability. It will test specific theory-guided hypotheses to determine the various ways brain regions more greatly interact throughout adolescent maturation to produce improvements in executive control. Because of the increasing recognition of the importance of widely-distributed, functionally-integrated neural networks in complex cognition, this project will conduct the first systematic assessment of neural functional connectivity underlying executive function. In this supplement, we request funds to add diffusion tensor imaging (DTI) assessment of our sample to the project to permit quantification of developmental changes in anatomical connectivity. We also will collect ´resting state´ fMRI scans to permit an expanded look at functional connectivity relative to the executive fMRI tasks, and relative to an analysis of our archival database of resting state/DTI scans. Most importantly, we will integrate the DTI data into a working measurement model that seeks to determine the influence of maturing functional and anatomical connectivity on cognitive development. By adding DTI within the analytic framework of the funded project, we hope to greatly extend the pace and theoretical impact of our research. PUBLIC HEALTH RELEVANCE Although impairment in ´executive´ cognitive functions is associated with risk for numerous psychiatric disorders that often arise in adolescence, there is insufficient understanding of the neural basis for these complex cognitive abilities. This project will provide the first large-scale study of executive control brain behavior relationships using functional neuroimaging of network functional integration, cognitive testing, and imaging of brain volume and white matter connectivity to depict neurobiological changes associated with normal development of ´adult-level´ cognitive ability. In addition to clarifying numerous unanswered questions about the development of executive control, the information provided by this project will benefit future clinical neuroscience studies seeking to better understand cognitive risk factors that contribute to psychiatric illness
Keywords: 12-20 years old; 21+ years old; AD/HD; ADHD; Address; Adolescence; Adolescent; Adolescent Development; Adolescent Youth; Adult; Affect; Age; Anterior; Attention deficit hyperactivity disorder; Attention-Deficit Disorder, Predominantly Hyperactive-Impulsive Type; Autism; Autism, Early Infantile; Autism, Infantile; Autistic Disorder; Award; BOLD response; Behavior; Biological Neural Networks; Brain; Brain region; Cell Communication and Signaling; Cell Signaling; Childhood; Classification; Clinical; Cognition; Cognitive; Complex; Conduct Disorder; Cross Sectional Analysis; Cross-Sectional Analyses; Cross-Sectional Studies; Cross-Sectional Survey; Data; Data Banks; Data Bases; Data Collection; Data Set; Databank, Electronic; Databanks; Database, Electronic; Databases; Dataset; Development; Diffusion MRI; Diffusion Magnetic Resonance Imaging; Diffusion Weighted MRI; Disease Frequency Surveys; Distal; Encephalon; Encephalons; Equation; Figs; Figs - dietary; Frequencies (time pattern); Frequency; Functional Magnetic Resonance Imaging; Funding; Future; Human, Adult; Hyperactivity Disorder NOS; Hyperactivity Disorder, Predominantly Hyperactive-Impulsive Type; Hyperkinetic Syndrome; Image; Impairment; Intracellular Communication and Signaling; Kanner`s Syndrome; Lateral; Learning; Linear Models; Link; Logic; MR Imaging; MR Tomography; MRI; MRI, Functional; Magnetic Resonance Imaging; Magnetic Resonance Imaging Scan; Magnetic Resonance Imaging, Functional; Measurement; Measures; Mediating; Medical Imaging, Magnetic Resonance / Nuclear Magnetic Resonance; Memory, Immediate; Memory, Short-Term; Memory, Shortterm; Mental disorders; Mental health disorders; Methods; Modeling; Models, Theoretic; Monitor; NMR Imaging; NMR Tomography; Nature; Nerve Cells; Nerve Unit; Nervous; Nervous System, Brain; Neural Cell; Neural Development; Neurobiology; Neurocyte; Neurons; Neuropsychologic Tests; Neuropsychological Tests; Neurosciences; Nuclear Magnetic Resonance Imaging; Operation; Operative Procedures; Operative Surgical Procedures; Parents; Parietal; Participant; Pattern; Performance; Prefrontal Cortex; Process; Psychiatric Disease; Psychiatric Disorder; Puberty; Relative; Relative (related person); Reporting; Research; Rest; Risk; Risk Factors; Sampling; Scanning; Schizophrenia; Schizophrenic Disorders; Scientist; Short-Term Memory; Signal Transduction; Signal Transduction Systems; Signaling; Specific qualifier value; Specified; Structure; Surgical; Surgical Interventions; Surgical Procedure; System; System, LOINC Axis 4; Systematics; Task Performances; Testing; Theoretical model; Time; Unspecified Mental Disorder; Work; Zeugmatography; adolescence (12-20); adult human (21+); adult youth; age dependent; age related; attention deficit hyperactive disorder; base; biological signal transduction; blood oxygenation level dependent response; brain behavior; brain volume; clinical data repository; clinical data warehouse; cognitive function; data repository; dementia praecox; depression; diffusion tensor imaging; endophenotype; executive control; executive function; expectation; experience; fMRI; frontal cortex; frontal lobe; hemodynamics; human puberty; imaging; improved; independent component analysis; infancy; infantile; juvenile; juvenile human; mental illness; myelination; neural; neural circuit; neural circuitry; neural control; neural model; neural network; neural regulation; neurobiological; neurodevelopment; neuroimaging; neuronal; neuropsychiatric; neuropsychiatry; neuroregulation; parent grant; parent project; pediatric; performance tests; psychological disorder; public health relevance; relating to nervous system; relational database; response; schizophrenic; substantia alba; surgery; teenage; theories; white matter; working memory; young adult
Relevance: Although impairment in ´executive´ cognitive functions is associated with risk for numerous psychiatric disorders that often arise in adolescence, there is insufficient understanding of the neural basis for these complex cognitive abilities. This project will provide the first large-scale study of executive control brain- behavior relationships using functional neuroimaging of network functional integration, cognitive testing, and imaging of brain volume and white matter connectivity to depict neurobiological changes associated with normal development of ´adult-level´ cognitive ability. In addition to clarifying numerous unanswered questions about the development of executive control, the information provided by this project will benefit future clinical neuroscience studies seeking to better understand cognitive risk factors that contribute to psychiatric illness
Project start date: 2009-09-30
Project end date: 2011-09-29
Budget start date: 30-SEP-2009
Budget end date: 29-SEP-2010
PFA/PA: PA-07-070
3R01MH081969-01A2S1 (2009): $326789
Sponsored Links Excellgen http://Excellgen.com
Michael C Stevens
Hartford Hospital
Project start date: 2008-05-15
Project end date: 2013-03-31