2008

Correction of Retardation and Autism in Mice Points to Human Treatment

Image
Mark Bear (right), director of thePicower Institute and PicowerProfessor of Neuroscience), andGu¨l Do¨ len, a graduate student atBrown University, report the correctionof fragile X syndrome inmice. (Donna Coveney)
Researchers at MIT’s Picower Institute for Learning and Memory have corrected key symptoms of mental retardation and autism in mice. Their findings indicate that a certain class of drugs could have the same effect in humans.

Fragile X syndrome (FXS), affecting 100,000 Americans, is the most common inherited cause of mental retardation and autism. The MIT researchers corrected FXS in mice modeling the disease. The findings support the theory that many of FXS’s psychiatric and neurological symptoms such as learning disabilities, autistic behavior, and childhood epilepsy, stem from too much activation of one of the brain’s chief network managers, the metabotropic glutamate receptor mGluR5. By reducing mGluR5, the excesses can be reduced.

Individuals with FXS have mutations in the X chromosome’s FMR1 gene, which encodes the fragile X mental retardation protein, FMRP. The MIT study found that FMRP and mGluR5 keep each other in check and, without FMRP, mGluR5 signals run rampant.

Find out more here.

White Papers

Stencil-less Jet Printing for PCB Assembly
Sponsored by Imagineering
Creating A New Category - Peelable FEP Heat Shrink Technology
Sponsored by Junkosha
Force Transfer Machines
Sponsored by Morehouse
Parallel Prototyping and the Engineer’s Dilemma
Sponsored by Heatron
Integrated Epoxy Feedthroughs Improve Fuel Pump Reliability
Sponsored by Douglas Electrical Components
HAIs and Chemical Resistance
Sponsored by Eastman

White Papers Sponsored By:

The U.S. Government does not endorse any commercial product, process, or activity identified on this web site.