Abstract
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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 133-140 |
| Number of pages | 8 |
| Journal | Journal of Neurodevelopmental Disorders |
| Volume | 1 |
| Issue number | 2 |
| DOIs | |
| State | Published - 2009 |
Keywords
- Angelman
- Audiogenic seizure
- Autism .HOMER
- BDNF
- Cognitive
- Cortex
- Dendritic spine
- Development
- Dominance
- Extinction
- FMRP
- FXS
- Fragile X
- Fragile x mental retardation protein
- Glutamate
- Hamartoma
- Hippocampus
- Impairment
- Inhibitory avoidance
- LTD
- Long term depression
- MeCP
- Mental retardation
- Metabotropic
- Mglur
- Mglur5
- Neurexin
- Neuroligin
- Ocular
- PTEN
- Passive avoidance
- Plasticity
- Protein synthesis
- Receptor
- Rett
- SHANK
- Seizure
- Synapse
- Synapsopathy
- Synaptic plasticity
- TSC
- TSC1
- TSC2
- Translation
- Tuberous sclerosis
- UBE3
- Visual
ASJC Scopus subject areas
- Pediatrics, Perinatology, and Child Health
- Pathology and Forensic Medicine
- Clinical Neurology
- Cognitive Neuroscience