| 2001 — 2005 |
Sobin, Christina |
K08Activity Code Description:
To provide the opportunity for promising medical scientists with demonstrated aptitude to develop into independent investigators, or for faculty members to pursue research aspects of categorical areas applicable to the awarding unit, and aid in filling the academic faculty gap in these shortage areas within health profession's institutions of the country. M01Activity Code Description:
An award made to an institution solely for the support of a General Clinical Research Center where scientists conduct studies on a wide range of human diseases using the full spectrum of the biomedical sciences. Costs underwritten by these grants include those for renovation, for operational expenses such as staff salaries, equipment, and supplies, and for hospitalization. A General Clinical Research Center is a discrete unit of research beds separated from the general care wards. |
Attention in Children With the 22q11 Deletion Syndrome
DESCRIPTION: (Adapted from the applicant's Description) This project proposes to assess attention in children whose genetic differences may underlie both attention deficits and neurotransmitter dysregulation. Children with the 22q11 deletion syndrome lack genes that encode two neuromodulators that specifically impact dopamine / glutamate / GABA pathways, catechol-O-methytransferase and proline dehydrogenase. Eighty to 100 percent of 22q11 deletion syndrome children are estimated to have learning disabilities and attention deficit. Segregated networks of attention have been localized in the human brain via imaging methods, and the neurochemical substrates of these networks have been suggested. This research aims to compare 22q11 deletion syndrome children and matched normal controls with regard to: 1) efficiency of three attention networks; 2) pre-pulse inhibition; 3) neuropsychological functioning, temperament and behavior. Findings will be used to further consider the neuroanatomical models of attention, to relate sensory motor gating to these models, and to characterize the association between attention deficits and neuropsychological performance, temperament, and disordered behavior.
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0.943 |
| 2009 — 2010 |
Sobin, Christina |
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.) |
Lead, Genes, and Cognition in Underserved Children @ University of Texas El Paso
DESCRIPTION (provided by applicant): The goal of this work is to begin to identify biological mechanisms that contribute to neurocognitive deficits in children exposed to low-level lead. This research plan proposes to measure blood lead levels in a large population of minority and underserved children;compare neurocognitive functioning in children with and without detectable blood lead levels;and examine associations between selected genetic polymorphisms and neurocognitive performance in children exposed to low-level lead. Lead exposure is a significant health disparity. Low-level lead exposure has long been associated with diminished cognitive function, and may pose an unrecognized threat to the cognitive health and well-being of an unknown number of minority and underserved children. Moreover, previously unexamined common genetic differences may potentiate the neurotoxic effects of lead in children. Lead toxicity is diagnosed when a child's blood lead level (BLL) is >10 micrograms per deciliter (g/dL). According to the EPA however, a "Reference Dose" value, that is a concentration below which no adverse effects have been observed, is not available for lead. In response to over 40 studies showing diminished IQ in children with BLLs <10 g/dL, the CDC convened an expert committee in 2003 to critically examine the findings. The findings were unequivocally confirmed. But in its decision to maintain the 10 g/dL threshold, the committee cited the need for studies suggesting causative biological mechanisms. We do not yet understand the mechanisms by which low-level lead exposure causes neurocognitive decline in young children. This is a critical knowledge gap, which creates the risk of lower cognitive function and diminished quality of life, especially for minority and underserved children. As a result of this gap, child blood lead levels <10.0 g/dL are ignored. Our central hypothesis is that chronic low-level lead exposure impairs neurocognitive function through mechanisms that are genetically mediated. H1: 25% of minority children between the ages of 5 and 12 have "detectable" blood lead levels (4.0 - 9.9 g/dL);H2: as compared to children with "undetectable" blood lead levels, children with "detectable" blood lead levels perform more poorly on neurocognitive tasks associated with brain networks specifically vulnerable to lead;H3: children with "detectable" blood lead levels, and carrying one or both genetic polymorphisms, have lowest scores on tests of neurocognitive function. Findings from these studies may begin to suggest the numbers of minority and underserved children ages 5 - 12 currently exposed to low-level lead;which types of neurocognitive deficits result;and whether common genetic differences potentiate the neurotoxic effects of lead. The findings may also suggest new avenues for detection, primary prevention and intervention. PUBLIC HEALTH RELEVANCE: Lead exposure is a significant health disparity, low-level lead exposure has been associated with diminished cognitive function, and yet low-level lead exposure continues to be ignored, perhaps posing a hidden threat to the health and well-being of an unknown number of minority and underserved children. Common genetic differences may increase its neurotoxic effects. Findings from these studies may begin to suggest the numbers of currently exposed minority and underserved children ages 5 - 12 years, and which neurocognitive deficits result, while suggesting new avenues for detection and primary prevention.
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