There’s finally some new news in Autism Spectrum Disorder (ASD) research. Under the direction of Drs. João Peça and Cátia Feliciano at Duke University (Neurobiology department), the research group have created “autistic” mice. Why is that important? Without having a valid animal model for the disease, it is difficult to afford quick and safe testing of various regimens to treat ASD. The problem, heretofore, has been to find a key factor behind the development of ASD. This is because a plethora of genes have been linked to ASD, which means too many combinations were needed to develop a study model; moreover, individual ASD patients demonstrated different combinations of these genes.
As the scientists reported in Nature, a protein, Shank3, seems to key factor in the manifestation of ASD. How? It precludes the proper communication among brain cells. Shank3 is present in the synapses (the space between neurons in which nerves communicate with one another via chemical messengers). (In technical terms, this protein, when disrupted at the genetic level, is involved with the Phelan-McDermid Syndrome (22q13 deletion syndrome) and other non-syndrome related ASD behaviors.) Once the mice were treated to disrupt the Shank3 protein, they demonstrated the classic symptoms of ASD- repetitive behavior (self-injurious grooming behaviors) and other social networking problems.
This research was done in concert with Drs. Feng and Fu (McGovern Institute of Brain Research) of MIT. The MIT scientists analyzed the brains of the mice that were affected by the Duke team. They found that the “circuits” that connect the cortex and the striatum (cortex means outer layer; striatum is the inner layer) in the mice brain had defects. This “circuit” is considered to be the regulator of social behaviors and interactions. As such, the first animal model for ASD is verified.
It should be noted that Shank3 is probably NOT the controlling factor in humans who develop ASD. However, based upon this research, it is probably that this and other proteins that are responsible for the proper communication among synapses of neurons are the key factors. As such, developing a treatment that restores proper synaptic function (regardless of the specific cause) is the key modality for future research.
Roy, it’s great to meet you over the World Wide Web! =) I’ve noticed you around the blogging world, thought I’d stop by and loved your varied content!
I’ve been involved with research in autism myself (more cognitive and behavioural), so I’m equally excited about the prospects of mice models! I’m curious whether these models also apply to HFA and Asperger’s, that seem to be establishing themselves as separate disorders these days.
Looking forward to reading more! =)
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I am so glad you dropped in, Samantha. Give me some notice next time and I will have some coffee ready for you :-).
Thanks for your comment. Hopefully, this will help you in your work as well.
Have a great day!
Roy,
I have several friends and a client who has children with various degrees of Autism!
I’m not a scientific person, but curious this protein…where does it come from and I know you said this doesn’t prove for humans, but if it does, how do we make sure our kids don’t get it or whatever it is?
I, too, have intimate knowledge of the affliction. This protein is part of the normal process. By altering it, the transfer of neurotransmitters acrosss synapses is affected. It is not THE cause of ASD. Rather, it may be one of many potential synapse alteration chemicals that leads to the lack of transmission of information- or the transmission of an altered message- that leads to the manifestation of ASD.
We do NOT know the cause of ASD. As stated in this article (and my other ones), there are multiple potential causes. They may or may not mediate the utlimate level of progression of symptoms. More needs to be determined. (Just like cancer is not caused by one mutation or one gene.)
I have no knowledge about autism but so appreciate the wide range of topics you write on. You did a great job of making a complex, scirentific topic understandable whie spreading good news of progress.
Glad you like it, Tambre! That’s the job for every advisor- provide information in a means that the recipient can understand and employ.
Thanks for the compliment.
Roy, this is interesting and very promising in my non-scientific mind :). Possibly finding the key factor behind the development of Autism Spectrum Disorder is huge and the fact that the symptoms can now be replicated in animals is significant. If it’s that a protein messes up communication between or among synapses . . . and if that problem is treated successfully . . . ASD could be completely eliminated.
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Leanne:
That’s exactly what is needed! One can only hope that progress progresses :-)!
That’s what one hopes for when developing animal models. (Sorry, PETA, this is still among the best ways to test out treatment regimens.)
The more we know sometimes the less we know. It is interesting that the increase is so many diseases is because of the change of diet that means certain things don’t happen. I have followed some of this research for years and autism is one disease that mother’s controlling diet have had major effects so no surprise that researchers found it was protein based. I know that many seeming diseases and conditions are caused by the foods we eat or their combination. Thanks for another interesting article Roy
Glad you enjoyed it, Roberta. However, there is virtually no possibility that one’s choice of diet will cause these protein defects.
Roy, I do not understand the “scientific” info which you are referring too, but I am hopeful for any research that gets us closer to helping individuals with autism. This cause is very near and dear to my heart!
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Thanks for your note. If you can provide a question, I will attempt to answer it to insure your comprehension.
Take care,
Roy
Thanks Roy! I will keep that in mind! Btw, I didn’t mean to put those quotations around the word scientific! I changed what I was going to say and forgot to remove them! 🙂
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Glad to oblige. Thanks. Jen!