Tropic Thunder Helps Those With Intellectual Disabilities

I am the father of a 12 year old boy diagnosed with Autistic Disorder and assessed with Profound Developmental Delays. I was invited to attend a showing of Tropic Thunder and yesterday I did so, albeit with serious misgivings. Having seen the movie I believe that Tropic Thunder actually helps those with intellectual disabilities, and others, by focusing our attention on how the motion picture industry exploits, and presents inaccurate, and false, images of people with intellectual disabilities and other challenges, including obesity and addiction.


Tropic Thunder targets Hollywood for a number of sins, including its exploitation and presentation of distorted images of people with intellectual disabilities. The character portrayed in the movie within the movie, "Simple Jack", does not resemble in any way anyone I have ever met with an intellectual disability or developmental delay. The presentation of the character and the use of the word "retard" in some of the relevant scenes was uncomfortable for me as the father of a son with "profound developmental delays". But I did not find it offensive. and the clear targets are the vain and superficial actors who portray such distortions and the industry which greedily exploits them.

I am not trying to tell others how to feel about this issue. Or whether they should see the movie. For me, Tropic Thunder raised serious issues for discussion in the way that satire does - not by a scholarly dissertation - but by actually showing, and mocking, its target - in this case the motion picture industry.

And it is funny.

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Autism Disorder Versus Asperger's Syndrome

The Autism Society of America has published a good overview of Autism Disorder and Asperger's Syndrome on TylerPaper.com. The article contains a basic description of both Autism Disorder and Asperger's Syndrome and helps distinguish between the two similar but distinct disorders:

What distinguishes Asperger's Syndrome from autism is the severity of the symptoms and the absence of language delays. To the untrained observer, a child with Asperger's may seem just like a normal child behaving differently. They may be socially awkward, not understanding of conventional social rules, or show a lack of empathy. They may make limited eye contact, seem to be unengaged in a conversation, and not understand the use of gestures.

One of the major differences between Asperger's Syndrome and autism is that, by definition, there is no speech delay in Asperger's. In fact, children with Asperger's frequently have good language skills; they simply use language in different ways. Speech patterns may be unusual, lack inflection, or have a rhythmic nature or it may be formal, but too loud or high pitched. Children with Asperger's may not understand the subtleties of language, such as irony and humor, or they may not recognize the give-and-take nature of a conversation.

Another distinction between Asperger's Syndrome and autism concerns cognitive ability. While some individuals with autism experience mental retardation, by definition a person with Asperger's cannot possess a "clinically significant" cognitive delay, and most possess average to above-average intelligence.

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Study Details Atomic Structure of Autism Associated Proteins

Autism has been defined largely by behavioral deficits. That is changing though as new research is reported almost daily providing more detail on the neurological basis of autism. NEURON magazine in its incredible December 20 07 issue has published a report of a study showing it is possible to reverse some symptoms of Fragile X and some autism disorders. The same issue reports a study detailing, on an atomic level, the structure of altered proteins associated with autism.

In Structural Analysis of the Synaptic Protein Neuroligin and Its b-Neurexin Complex:
Determinants for Folding and Cell Adhesion Pascale Marchot and Igor P. Fabrichny, Institut Fédératif de Recherche-Jean Roche, Université de la Mediterranée; Philippe Leone, Gerlind Sulzenbacher and Yves Bourne, Universités Aix-Marseille; and Davide Comoletti and Meghan T. Miller, UCSD Department of Pharmacology, Skaggs School of Pharmacy and Pharmaceutical Sciences provide detailed data, charts and description of the structure of the neurologin family of proteins believed to be affected by genetic mutations and believed to be involved with autism and mental retardation.

In Atomic Structure of Proteins Altered in Autism the University of California, San Diego Health Sciences Press Release published on Newswise emphasizes that this study builds on previous studies but provides new detail:

“This goes beyond previous studies to show the individual atoms of these two proteins and how they interact,” said Palmer Taylor, Ph.D., Dean of SSPPS and the Sandra & Monroe Trout Professor of Pharmacology. “We have described the mutations found in some people with autism; and we have identified where the altered amino acids are located in the protein, and how they impact the folding and cell adhesion properties of neuroligin and neurexin.”

The research builds on earlier work that mapped the molecular structure of neuroligins and their partner proteins, neurexins – a protein complex involved in the junctions, or synapses, through which cells of the nervous system signal to one another. The new study, conducted with Pascale Marchot and Yves Bourne and their colleagues in Marseille, France, adds to a clearer understanding of how particular genetic mutations affect formation of this complex and contribute to the developmental abnormalities found in certain individuals with autism.

Normally, individual neuroligins interacting with specific neurexin partners are involved in synaptic adhesions, imparting ‘stickiness’ that enables them to associate and form synapses that have the capacity for neurotransmission. Incorrect partnering in these diverse protein families results when a mutant neuroligin fails to associate properly at synapses, preventing the normal transmission of brain cells.

The change in synaptic function may account for impairments in development, social interaction and communication displayed in individuals with autism spectrum disorders, according to the researchers.

The world is experiencing an Autism Knowledge Revolution. When knowledge grows superstition, prejudice, ideology and personal agendas wane in influence, in this case to the benefit of persons with autism.

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Autism May Result from Wrong Amount of MeCP2 Protein, Wrong Number of Synapses

“MeCP2 has an important role in fine-tuning the amount of synaptic responses, having just the right amount of MeCP2 and the right number of synapses drives healthy brain development"

- Hsiao-Tuan Chao, M.D./Ph.D. graduate student, Baylor College of Medicine

A study published in Neuron reports evidence that problems in synapse formation early in post natal development give rise to mental retardation, Rett syndrome, autism and other developmental disorders. The protein MeCP2 (methyl-CpG binding protein 2) is critical in determining the number of synapses. And the correct number of synapses is necessary for healthy brain development. A mutation of the MeCP2 gene results in too little of the protein which further results in girls developing Rett syndrome. Boys with too much MeCP2 have spasticity and mental retardation with autism-like behavior.

In MeCP2 Controls Excitatory Synaptic Strength by Regulating Glutamatergic Synapse researchers Hsiao-Tuan Chao, Huda Y. Zoghbi, and Christian Rosenmund of the Baylor College of Medicine report conclusions of their study of two groups of mice, one group of mice with too little MeCP2, and another group with too much of the protein, to figure out what is the right number of synapses and how the number is determined. The found that too little of the MeCP2 protein meant that not enough synapses formed. Too much MeCP2 meant too many synapses formed.

As reported on the Baylor College of Medicine web site:

“The beauty of this result is that this critical process in the development of synaptic connectivity in the brain is tightly regulated by the amount of MeCP2,” said Rosenmund. “It is one of the strongest pieces of evidence that mental retardation and autism-like diseases originate with problems in synapse formation.”

Chao said, “It suggests that the pathways in which MeCP2 is involved and the proteins it regulates are probably critical for how the brain can determine how many synapses to make as it’s developing.”

“This determination of how many synapses to make happens early in life,” said Zoghbi. “If it’s not right, then the brain undergoes secondary changes to try to compensate. This is a big important observation and opens up ways to think about adult diseases that involve loss of synaptic function. It is also interesting that patients who lack this protein or have too much have features of autism. More and more, data point to the possibility that autism is a disorder of abnormal function of the synapse.”

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