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High-probability grants
According to our matching algorithm, Paolo Moretti is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
2002 — 2004 |
Moretti, Paolo |
F32Activity Code Description: To provide postdoctoral research training to individuals to broaden their scientific background and extend their potential for research in specified health-related areas. |
Pathogenesis of the Movement Disorders of Rett Syndrome @ Baylor College of Medicine
DESCRIPTION (provided by applicant): Rett syndrome (RTT), a leading cause of mental retardation in females, causes cognitive, motor, and social regression after an initial period of normal development. Movement disorders and stereotypical hand behavior are distinctive features in these patients. RTT is caused by loss of function mutations in the X-linked gene encoding methyl-CpG binding protein 2 (MeCP2), a transcriptional repressor that binds to methylated CpG dinucleotides. Abnormalities of the basal ganglia and dopaminergic transmission have been described in RTT, but the molecular events leading from mutation of MeCP2 to the neurologic deficits of this disorder are unknown. I am interested in the role of the basal ganglia in RTT and the function of MeCP2 and DNA methylation in these sub cortical structures. I hypothesize that specific neuronal abnormalities of gene expression in the basal ganglia are at the root of the movement disorders of RTT. I propose to use Mecp2 mutant mice generated in Dr. Zoghbi 'S lab to identify genes that are misregulated in the basal ganglia. To pursue this study, I will (1) analyze motor and stereotypical behavior in mutant mice; (2) compare gene expression in the striatum and brainstem of wild-type and mutant mice using a candidate gene approach and cDNA micro array experiments; (3) study the effects of methyl-donors known to increase DNA-methylation on the mutant mouse phenotype. These studies will begin to shed light on the pathogenesis of RTT, and lend insight into the biology of mental retardations, movement disorders, and the role of DNA methylation in brain function.
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1 |
2005 — 2009 |
Moretti, Paolo |
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. |
Understanding Neuronal Dysfunction in Rett Syndrome @ Baylor College of Medicine
DESCRIPTION (provided by applicant): Rett syndrome (RTT) is an X-linked disorder caused by loss of function mutations in the MECP2 gene. RTT is a leading cause of mental retardation with autistic features in girls and is characterized by loss of acquired cognitive, motor and social skills. MECP2 mutations have also been shown to cause non-syndromic forms of mental retardation in both males and females. The methyl-CpG binding protein 2 (MeCP2) is a transcriptional represser that binds to methylated CpG dinucleotides. The molecular events resulting from dysfunction of MeCP2 and causing the neurologic deficits of RTT are unknown. Mecp2308/Y mutant mice generated in Dr. Zoghbi's lab are an excellent model to study the biological basis of this disorder. Dietary methyl donors can significantly modify the phenotype of these mice. This proposal aims to understand the cognitive and motor deficits of RTT by studying behavioral and functional abnormalities in the brain of mutant mice and investigating molecular mechanisms by which loss of MeCP2 function causes the RTT phenotype. It is based on the hypothesis that loss of MeCP2's function causes altered transcriptional regulation and abnormal expression of neuronal proteins required for synaptic plasticity. The specific aims are to: (1) Study Mecp2308/Y mice for learning and memory deficits; (2) Characterize electrophysiological abnormalities of synaptic plasticity in cortical and subcortical areas of the brain in mutant mice; (3) Identify genes that are abnormally expressed in affected brain regions of Mecp2308/Y mice and discover transcriptional changes associated with phenotypic improvement in response to a low methyl donor diet. These studies will begin to shed light on the cellular and molecular abnormalities of RTT and the role of methyl donors and DNA methylation in neuronal function. Key molecular regulators of cognition and motor function as well as modifiers of these neurologic phenotypes will be identified. These molecules will provide targets for the selection of rational treatment strategies in RTT and may be relevant to the study of neurologic diseases with overlapping phenotypes, such as autism and movement disorders.
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