[article]
| Titre : |
Dysregulation of fragile × mental retardation protein and metabotropic glutamate receptor 5 in superior frontal cortex of individuals with autism: a postmortem brain study |
| Type de document : |
Texte imprimé et/ou numérique |
| Auteurs : |
S. Hossein FATEMI, Auteur ; Timothy D. FOLSOM, Auteur |
| Année de publication : |
2011 |
| Article en page(s) : |
11 p. |
| Langues : |
Anglais (eng) |
| Index. décimale : |
PER Périodiques |
| Résumé : |
Background
Fragile × syndrome is caused by loss of function of the fragile × mental retardation 1 (FMR1) gene and shares multiple phenotypes with autism. We have previously found reduced expression of the protein product of FMR1 (FMRP) in vermis of adults with autism.
Methods
In the current study, we have investigated levels of FMRP in the superior frontal cortex of people with autism and matched controls using Western blot analysis. Because FMRP regulates the translation of multiple genes, we also measured protein levels for downstream molecules metabotropic glutamate receptor 5 (mGluR5) and γ-aminobutyric acid (GABA) A receptor β3 (GABRβ3), as well as glial fibrillary acidic protein (GFAP).
Results
We observed significantly reduced levels of protein for FMRP in adults with autism, significantly increased levels of protein for mGluR5 in children with autism and significantly increased levels of GFAP in adults and children with autism. We found no change in expression of GABRβ3. Our results for FMRP, mGluR5 and GFAP confirm our previous work in the cerebellar vermis of people with autism.
Conclusion
These changes may be responsible for cognitive deficits and seizure disorder in people with autism. |
| En ligne : |
http://dx.doi.org/10.1186/2040-2392-2-6 |
| Permalink : |
https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=131 |
in Molecular Autism > (May 2011) . - 11 p.
[article] Dysregulation of fragile × mental retardation protein and metabotropic glutamate receptor 5 in superior frontal cortex of individuals with autism: a postmortem brain study [Texte imprimé et/ou numérique] / S. Hossein FATEMI, Auteur ; Timothy D. FOLSOM, Auteur . - 2011 . - 11 p. Langues : Anglais ( eng) in Molecular Autism > (May 2011) . - 11 p.
| Index. décimale : |
PER Périodiques |
| Résumé : |
Background
Fragile × syndrome is caused by loss of function of the fragile × mental retardation 1 (FMR1) gene and shares multiple phenotypes with autism. We have previously found reduced expression of the protein product of FMR1 (FMRP) in vermis of adults with autism.
Methods
In the current study, we have investigated levels of FMRP in the superior frontal cortex of people with autism and matched controls using Western blot analysis. Because FMRP regulates the translation of multiple genes, we also measured protein levels for downstream molecules metabotropic glutamate receptor 5 (mGluR5) and γ-aminobutyric acid (GABA) A receptor β3 (GABRβ3), as well as glial fibrillary acidic protein (GFAP).
Results
We observed significantly reduced levels of protein for FMRP in adults with autism, significantly increased levels of protein for mGluR5 in children with autism and significantly increased levels of GFAP in adults and children with autism. We found no change in expression of GABRβ3. Our results for FMRP, mGluR5 and GFAP confirm our previous work in the cerebellar vermis of people with autism.
Conclusion
These changes may be responsible for cognitive deficits and seizure disorder in people with autism. |
| En ligne : |
http://dx.doi.org/10.1186/2040-2392-2-6 |
| Permalink : |
https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=131 |
|
Dysregulation of fragile × mental retardation protein and metabotropic glutamate receptor 5 in superior frontal cortex of individuals with autism: a postmortem brain study in Molecular Autism, (May 2011)
