New research studies have pointed to the synapse, an intercellular junction that is responsible for transferring information between neurons, as possibly being a cause of autism. Neuroscientists from Tufts University’s School of Medicine recently finished conducting research that revealed that the synapse cannot perform correctly if it’s isn’t supplied with enough of a certain protein. If the synapse cannot function properly, then a child’s learning and memory skills can be hindered. The protein is called adenomatous polyposis coli (APC).
Michele H. Jacob, senior author of the study, said: “Both sides of the synapse are finely tuned for efficient transmission; an imbalance on either side can negatively impact function, resulting in cognitive deficits. Our study reveals that APC forms a key protein complex in the postsynaptic neuron that also provides signals to direct synapse maturation in the presynaptic neuron, ensuring that the two sides of the synapse mature in concert to provide optimal function.”
While researchers are already aware that mutations in the genes for neuroligin and neurexin have links to autism, they hadn’t known what was behind the mutations. In their study, they blocked the APC protein, and the synaptic levels for neuroligin and neurexin decreased.
Madelaine Rosenberg, first author of the study and an affiliate of Tufts University’s School of Medicine said: “Our study also sheds light on a poorly-understood but essential process, the cross-talk that occurs between presynaptic and postsynaptic neurons. When we perturbed APC function on the postsynaptic side, we saw changes on both sides of the synapse, indicating that APC organizes a protein complex that communicates against the normal flow of traffic.”
Source: Tufts University, Health Sciences. “Autism and Mental Retardation Connected With APC Protein.” ScienceDaily 24 August 2010. 25 August 2010 <http://www.sciencedaily.com /releases/2010/08/100823113426.htm>.