Journal
JOURNAL OF NEURODEVELOPMENTAL DISORDERS
Volume 1, Issue 2, Pages 133-140Publisher
BIOMED CENTRAL LTD
DOI: 10.1007/s11689-009-9015-x
Keywords
Fragile X; FXS; Metabotropic; Glutamate; Receptor; mglur; mglur5; FMRP; Fragile x mental retardation protein; Synaptic plasticity; Long term depression; LTD; Protein synthesis; Translation; Ocular; Dominance; Plasticity; Visual; Cortex; Hippocampus; Inhibitory avoidance; Passive avoidance; Extinction; Autism; HOMER; SHANK; Neuroligin; Neurexin; Tuberous sclerosis; TSC; TSC1; TSC2; Rett; MeCP; BDNF; PTEN; Hamartoma; Angelman; UBE3; Dendritic spine; Synapse; Development; Synapsopathy; Audiogenic seizure; Seizure; Mental retardation; Cognitive; Impairment
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Autism is an umbrella diagnosis with several different etiologies. Fragile X syndrome (FXS), one of the first identified and leading causes of autism, has been modeled in mice using molecular genetic manipulation. These Fmr1 knockout mice have recently been used to identify a new putative therapeutic target, the metabotropic glutamate receptor 5 (mGluR5), for the treatment of FXS. Moreover, mGluR5 signaling cascades interact with a number of synaptic proteins, many of which have been implicated in autism, raising the possibility that therapeutic targets identified for FXS may have efficacy in treating multiple other causes of autism.
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