Scientists have previously posited that autism’s cause is at the synapse. Mutations in the genes for neuroligins—which ensure that signal transitions between nerve cells function—-have been suggested as a cause of autism.  Neuroscientists at Children’s Hospital Boston have identified what is being called a “master switch” that organizes the functioning of inhibitory synapses. Synapses are the connections between brain cells and enable communication among neurons; they’re essentially for virtually all brain functions, such as memory, sensory perception, motor coordination, learning.
The “master switch” is Npas4, which is a transcription factor, a “switch” that activates or represses other genes; it regulates …read more

About one-third of those with Fragile X also have autism. My son was tested for Fragile X around the time that he was being evaluated for autism, and Charlie does not have Fragile X (go here to read about a new gene that was found for Fragile X earlier this year). A recent study in Developmental Cell has found that those with Fragile X lack a protein that is crucial for the signaling between the nucleus of neurons and the synapse; this protein is essential for brain development, memory, and learning. More in today’s Science Daily and more about the …read more

MIT researchers have found that the lack of a brain protein, Shank 1, in mice causes them to learn some tasks faster but, when tested weeks later, they were not able to retain that knowledge. Shank 1 is a key protein in building synapses, and mutations in the closely related protein, Shank 3, have been linked to autism. The mice were found to be able to learn a spatial task quickly but (as compared to normal mice) were later unable to remember how to do it. The study is published in the Journal of Neuroscience; here are more details form …read more