Guest guest Posted June 27, 2008 Report Share Posted June 27, 2008 FYI, It was proposed in 1997 that neuroprotein manufacturing processes and, the amygdale are involved in identifying the etiology of Autism. 11 years later, it is more than just a hypothesis. See below, From: sarnets-bounces@... On Behalf Of schafer Sent: Wednesday, June 25, 2008 1:47 PM To: Schafer Autism Report Subject: Postech May Unlock A Secret to Autism Wednesday, June 25, 2008 Reader Supported Vol. 12 No. 93p In This Issue: • RESEARCH Postech May Unlock A Secret to Autism • PUBLIC HEALTH NPR: Raw Milk: Panacea or Poison? • • • • • PEOPLE Autism Boy Jumps To Death Over Cancelled School Trip Computer Program Helped Find Autistic Man Missing Autistic Wisconsin Man Man, 21, Accused of Molesting Autistic Boys Mother of Autistic Child Puts Priest On Stand • FINANCE Autistic Australian Children To See $190m Support • • • • MEDIA The Autism File Magazine Debuts In The Us & Canada Kirby on WOR Radio in New York EVENTS National Autism Association' s National Autism Conference COMMENTARY The “Dark Age Of Autism” Is Dead LETTERS Vaccine Action DEADLINE TODAY! WEDS. June 25 For July Autism Events Calendar Submit listing here free! the Autism Calendartm here Hundreds of Local Autism Events RESEARCH Postech May Unlock A Secret to Autism By Ha. tinyurl.com/3nk4rf A team of researchers at Korea's Pohang University of Science and Technology (Postech) has found new clues in understanding the development process for autism, a brain disorder that impairs social interaction and communication skills. Kim Joung-Hun, a life sciences professor at Postech, and his research team have found a brain mechanism through which the disorder is created. The new finding was published this week by Proceedings of the National Academy of Sciences. Professor Kim and his team have found that a shortage of protein called " neuroligin " secreted by amygdala may lead to the brain disorder. Amygdala is an almond-shaped structure in the brain, involved in the generation of emotions and memories. The Postech research team said the shortage of neuroligin can interfere with normal activities between neurons and their synapses, leading to the onset of autism. " Neuroligin-1 is a potent trigger for the de novo formation of synaptic connections, and it has recently been suggested that it is required for the maturation of functionally competent excitatory synapses, " according to the findings. The research team manipulated brain chemicals of laboratory mice to mimic this condition. When laboratory mice no longer produced neuroligin protein in their brains, their neuron synapses' functional speed and adaptability dropped markedly. Such deterioration in brain synapses leads to autistic symptoms. This is reportedly the first time that a link between neuroligin protein and autism has been demonstrated. The research team says the finding will help further the understanding of autistic development in human brains and in developing possible treatments for the disorder. For rest of today's SAR click here: www.sarnet.org/frm/forsar.htm Today's SAR is provided through the support of paid subscription readers. - THANK YOU - $35 for 1 year - or free! www.sarnet.org Copyright Notice: The above items are copyright protected. They are for our readers' personal education or research purposes only and provided at their request. Articles may not be further reprinted or used commercially without consent from the copyright holders. To find the copyright holders, follow the referenced website link provided at the beginning of each item. Lenny Schafer editor@... The Schafer Autism Report is a non-profit corporation Unsubscribe here: www.sarnet.org/frm/unsub2.htm _______________________________________________ SARnets mailing list SARnets@... http://lists.igc.org/mailman/listinfo/sarnets You can unsubscribe send email: http://www.sarnet.org/frm/unsub2.htm -- You are subscribed as: kindergration@... No virus found in this incoming message. Checked by AVG. Version: 7.5.524 / Virus Database: 270.4.1/1519 - Release Date: 6/25/2008 4:13 PM Quote Link to comment Share on other sites More sharing options...
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