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

How To Guide for the Most Common Measurements
Sponsored by National Instruments
Bearing selection for low-speed applications
Sponsored by Kaydon
Re-Inventing the Rotary Encoder: The No-Compromise IXARC from POSITAL
Sponsored by Fraba Posital
Improving Absorption Measurements through Light Source Selection
Sponsored by Ocean Optics
High-Speed A/Ds for Real-Time Systems
Sponsored by Pentek
Medical Capabilities Brochure
Sponsored by Nordson EFD

White Papers Sponsored By: