Abstract
Fragile X syndrome, the most common known cause of inherited mental retardation, is caused by alterations of the FMR1 gene encoding the FMRP protein. We investigated the relation between FMRP protein levels and functional brain activation during a working memory task. Our study provides the first evidence for a relation between FMR1 gene expression and neural activity during higher-order cognition. More broadly, our findings provide the first demonstration of how gene-brain-behavior investigations can help to bridge the gap between molecular and systems neuroscience.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adolescent
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Adult
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Cerebral Cortex / metabolism
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Cerebral Cortex / pathology
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Cerebral Cortex / physiopathology*
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Child
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Cognition Disorders / genetics
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Cognition Disorders / pathology
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Cognition Disorders / physiopathology*
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Female
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Fragile X Mental Retardation Protein
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Fragile X Syndrome / metabolism
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Fragile X Syndrome / pathology
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Fragile X Syndrome / physiopathology*
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Gene Expression Regulation, Developmental / genetics
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Humans
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Magnetic Resonance Imaging / methods
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Memory, Short-Term / physiology
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Nerve Tissue Proteins / genetics
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Nerve Tissue Proteins / metabolism*
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Neuropsychological Tests
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Psychomotor Performance / physiology
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RNA-Binding Proteins*
Substances
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FMR1 protein, human
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Nerve Tissue Proteins
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RNA-Binding Proteins
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Fragile X Mental Retardation Protein