"Our results suggest that FKPB12 regulates neuron signaling that curbs the manifestation of traits observed in several neurological disorders including autism, obsessive-compulsive disorder and schizophrenia.These disorders are widely believed to be "determined in utero by genetic hormonal and environmental factors. Because our study indicates that postnatal release of mTOR activity can result in certain perseverative behaviors, it challenges the idea that some aspects of these conditions are developmentally predetermined."
- AFP, NYU neuroscientist Dr. Eric Klann
Autism clearly has a strong genetic component. Some believe it is entirely genetic with no environmental causes or factors. Those who subscribe to the "entirely genetic" belief find it easy to believe that the astonishing rise in the numbers of autism disorder diagnoses is due entirely to diagnostic definition changes, enhanced public awareness and other social factors. If they are wrong in their beliefs, and if scientific researchers and health authorities refuse to investigate potential environmental causes or triggers of autism then possible treatments, cures or enhancements of the lives of autistic people will be sacrificed on the alter of such unwarranted certainty.
From the erroneous and harmful "Refrigerator Mother" beliefs of Bettelheim to the belief that autism arises solely from genetic factors our popular understanding of, and ability to treat and cure, autism disorders have been restricted by simplistic, single factor explanations of the complex group of pervasive developmental, or autism spectrum, disorders. Recently though there has begun an autism research paradigm shift based on the view that:
"autism is not a rare disorder with a constant rate but frequent condition with a rising incidence. It is a combination of environmental influence and genetic vulnerabilities. It is both preventable and treatable, not by any one method but by a combination of behavioral and biomedical approaches. Autistic kids are not defective, they are sick but otherwise normal kids, and thus, recoverable."
A significant example of the autism research paradigm shift can be seen in the recent study authored by researchers at New York University's Center for Neural Science and the Baylor College of Medicine and published in Neuron,Volume 60, Issue 5, 832-845, 10 December 2008. The researchers studied the effects on mice of removal of the FK506-binding protein 12 (FKBP12) which regulates an enzyme (mTOR) involved in learning and memorization. mTOR affects the the ability to change behavior and regulates connections between neurons thereby playing a key role in learning and memorization.
As stated on AFP News, removal of FKBP12 from the brains of mice late in development reduced the mice's capacity to analyze, respond and adapt to new situations. In one example the FKBP12 removed mice, once they learned a path through a maze, had difficulty learning how to travel through a different version of the maze. The AFP article describes this phenomenon as "enhanced perseveration, or pathological repetition, ... often observed in individuals suffering from autism or other neurological disorders".
The Autism Research Paradigm Shift is a central component of the Autism Knowledge Revolution now taking place. Hopefully, that revolution in learning and understanding autism disorders will not be derailed or slowed by the world's current economic crisis ... or by ideologies, agendas and simplistic views of autism disorders.