Researchers debut the SHANK2 mouse and SHANK3 rat at the 2011 Society for Neuroscience annual meeting. SHANK2 belongs to the same family as SHANK3, a well-established autism candidate gene.
Loss of FMR1 function is the most common genetic cause of autism. Understanding how this gene works is vital to finding new treatments to help Fragile X patients and others...
Research team from Beth Israel Deaconess Medical Center (BIDMC) has created a genetically engineered mouse with increased dosages of the Ube3 gene. And, like the patients who also harbor increased dosages of this single gene, the genetically engineered mice exhibit robust examples of all three traits considered hallmarks of autism: reduced social interaction, impaired communication and excessive repetitive behaviors. Findings provide further clues in understanding the brain defects that lead to the development of autism, and offer an important tool for future use by scientists and clinicians to test possible drug therapies.
Scientists at Cold Spring Harbor Laboratory (CSHL) have discovered that one of the most common genetic alterations in autism -- deletion of a 27-gene cluster on chromosome 16 -- causes autism-like features. By generating mouse models of autism using a technique known as chromosome engineering, CSHL Professor Alea Mills and colleagues provide the first functional evidence that inheriting fewer copies of these genes leads to features resembling those used to diagnose children with autism.
A new strain of mice engineered to lack a gene with links to autism displays many of the hallmarks of the condition. It also responds to a drug in the same way as people with autism, which might open the way to new therapies for such people.
The first transgenic mouse model of a rare and severe type of autism called Timothy Syndrome is improving the scientific understanding of autism spectrum disorder in general and may help researchers design more targeted interventions and treatments.
This study examined mouse neuronal cells during pregnancy to discover how the drug actually interferes at a molecular level with prostaglandins, which are important for development and communication of cells in the brain.
Researchers at the Center for Translational Social Neuroscience (CTSN) at Emory University are focusing on prairie voles as a new model to screen the effectiveness of drugs to treat autism. They are starting with D-cycloserine, a drug Emory researchers have shown enhances behavioral therapy for phobias and also promotes pair bonding among prairie voles. Giving female voles D-cycloserine, which is thought to facilitate learning and memory, can encourage them to bond with a new male more quickly than usual.
With the help of two sets of brothers with autism, Johns Hopkins scientists have identified a gene associated with autism that appears to be linked very specifically to the severity of social interaction deficits. The gene, GRIP1 (glutamate receptor interacting protein 1), is a blueprint for a traffic-directing protein at synapses -- those specialized contact points between brain cells across which chemical signals flow.