Teach Effectively!

Gül Dölen and Mark Baer
Photo by Donna Coveney

Professor Mark Baer of the Massachusetts Institute of Technology (MIT), who studies how brains change as a result of experience, and his colleagues have identified bio-chemical factors (mGluR5 and FMRP) that, when re-balanced in mice bred to model Fragile-X syndrome, correct multiple defects associated with mental retardation and Autism. Here’s a snippet from the MIT press release:

Researchers at MIT’s Picower Institute for Learning and Memory have corrected key symptoms of mental retardation and autism in mice.

The work, which will be reported in the Dec. 20 issue of Neuron, indicates that a certain class of drugs could have the same effect in humans. These drugs are not yet approved by the FDA, but will soon be entering into clinical trials.

These sorts of findings are remarkable (silly me, I just remarked on it, didn’t I?) and encouraging. I look forward to future developments. To be sure, I presume that even if there were bio-physical corrections of the sort that these findings allow us to glimpse, there would still be the need for powerful educational manipulations.

Link to the press release and to an earlier story on this line of research.

Abstract from Neuron:

Correction of Fragile X Syndrome in Mice

Gül Dölen, Emily Osterweil, B.S. Shankaranarayana Rao, Gordon B. Smith, Benjamin D. Auerbach, Sumantra Chattarji, and Mark F. Bear1, ,

Received 29 March 2007; revised 8 October 2007; accepted 3 December 2007. Published: December 19, 2007. Available online 19 December 2007.

Summary

Fragile X syndrome (FXS) is the most common form of heritable mental retardation and the leading identified cause of autism. FXS is caused by transcriptional silencing of the FMR1 gene that encodes the fragile X mental retardation protein (FMRP), but the pathogenesis of the disease is unknown. According to one proposal, many psychiatric and neurological symptoms of FXS result from unchecked activation of mGluR5, a metabotropic glutamate receptor. To test this idea we generated Fmr1 mutant mice with a 50% reduction in mGluR5 expression and studied a range of phenotypes with relevance to the human disorder. Our results demonstrate that mGluR5 contributes significantly to the pathogenesis of the disease, a finding that has significant therapeutic implications for fragile X and related developmental disorders.