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Min, Kyung-Tai
Molecular & Cellular Neurobiology Lab(Min Lab)
Research Interests
  • Local protein synthesis, learning & memory, behavior, mitochondrial dynamics

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Meeting at the crossroads: common mechanisms in Fragile X and Down syndrome

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Title
Meeting at the crossroads: common mechanisms in Fragile X and Down syndrome
Author
Chang, Karen T.Ro, HyunahWang, WeiMin, Kyung-Tai
Keywords
MENTAL-RETARDATION PROTEIN; LONG-TERM DEPRESSION; AMYLOID PRECURSOR PROTEIN; DENDRITIC SPINE ABNORMALITIES; ALTERED SYNAPTIC PLASTICITY; NEURAL PROGENITOR CELLS; MESSENGER-RNA; MOUSE MODEL; TRANSGENIC MICE; ALZHEIMERS-DISEASE
Issue Date
201312
Publisher
ELSEVIER SCIENCE LONDON
Citation
TRENDS IN NEUROSCIENCES, v.36, no.12, pp.685 - 694
Abstract
Intellectual disability is characterized by significantly impaired cognitive abilities and is due to various etiological factors, including both genetic and non-genetic causes. Two of the most common genetic forms of intellectual disability are Fragile X syndrome (FXS) and Down syndrome (DS). Recent studies have shown that proteins altered in FXS and DS can physically interact and participate in common signaling pathways regulating dendritic spine development and local protein synthesis, thus supporting the notion that spine dysmorphogenesis and abnormal local protein synthesis may be molecular underpinnings of intellectual disability. Here we review the molecular constituents regulating local protein synthesis and spine morphology and their alterations in FXS and DS. We argue that these changes might ultimately affect synaptic homeostasis and alter cognitive performance.
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DOI
http://dx.doi.org/10.1016/j.tins.2013.08.007
ISSN
0166-2236
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