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• W2055460432 abstract "Dysfunctions of the geniculo-striatal magnocellular (M) visual pathway and its cortical recipients have been documented in fragile X syndrome and in FMR1 premutation carriers. However, the mechanism of this impairment is less clear. To elucidate this issue, we completed the measurement of visual functions at different stages of information processing: low-level mechanisms (contrast sensitivity biasing information processing toward the M and parvocellular [P] pathways), primary visual cortex (motion-defined and static Vernier threshold), and higher-level form and motion processing (coherence thresholds). Results revealed that FMR1 premutation carriers, relative to non-carrier controls, exhibited lower contrast sensitivity for M pathway-biased stimuli, higher Vernier threshold for motion-defined stimuli, and higher global motion coherence threshold. Although both elevated FMR1 mRNA and reduced fragile X mental retardation protein (FMRP) levels were associated with impaired visual functions, regression analysis indicated that FMRP was the primary factor. In premutation carriers, a toxic gain-of-function of elevated FMR1 mRNA has been suggested, whereas reduced FMRP is linked to neurodevelopmental aspects. Here, we showed that FMRP may the primary factor associated with visual dysfunctions." @default.
• W2055460432 created "2016-06-24" @default.
• W2055460432 creator A5026179396 @default.
• W2055460432 creator A5054680495 @default.
• W2055460432 date "2012-03-01" @default.
• W2055460432 modified "2023-09-24" @default.
• W2055460432 title "Why is vision impaired in fragile X premutation carriers? The role of fragile X mental retardation protein and potential FMR1 mRNA toxicity" @default.
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• W2055460432 doi "https://doi.org/10.1016/j.neuroscience.2012.01.005" @default.
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