Autism future or investigational therapies
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Future or Investigational Therapies
Proposed Models
Twin and family studies show that autism is a highly heritable condition, but they have left many questions for researchers, most notably
- Why is fraternal twin concordance so low considering that identical twin concordance is high?
- Why are parents of autistic children typically non-autistic?
- Which factors could be involved in the failure to find a 100% concordance in identical twins?
- Is profound mental retardation a characteristic of the genotype or something totally independent?
Some researchers have speculated that what we currently refer to as "autism" may be a catch-all description for many yet unknown conditions with different genetic and/or environmental etiologies. This would appear to make the effort to find a genotype model a lot more difficult, and perhaps even pointless. Nevertheless, a number of genetic models have been proposed to try to explain the results of twin and sibling studies.
Isodicentric Chromosome 15 and Autism
For more than 12 years, scientists have noticed that some individuals with autism also have idic(15). In fact, idic(15) is the most frequently identified chromosome problem in individuals with autism. (A chromosome anomaly involves extra or missing chromosomal material, not changes within the genes such as Fragile X syndrome). It is suggested that the co-occurrence of autism and idic(15) is not by chance. There may be a gene or genes in the 15q11-q13 region that is/are related to the development of autism in some individuals.
Genetic research studies of individuals without chromosome anomalies also support this idea that an autism-related gene may be present in 15q11-q13. Specifically, research studies found that certain DNA markers from the 15q11-q13 region were found more often in individuals with autism than in individuals without autism. Although these DNA markers are too small to be genes, they suggest that researchers may be getting close to finding an autism gene in this region.
Mirror Neuron and Autism
Some researchers claim there is a link between mirror neuron deficiency and autism. In typical children, EEG recordings from motor areas are suppressed when the child watches another person move, and this is believed to be an index of mirror neuron activity. However, this suppression is not seen in children with autism [1]. Also, children with autism have less activity in mirror neuron regions of the brain when imitating [2]. Finally, anatomical differences have been found in the mirror neuron related brain areas in adults with autism spectrum disorders, compared to non-autistic adults. All these cortical areas were thinner and the degree of thinning was correlated with autism symptom severity, a correlation nearly restricted to these brain regions.[3] Based on these results, some researchers claim that autism is caused by a lack of mirror neurons, leading to disabilities in social skills, imitation, empathy and theory of mind. This is just one of many theories of autism and it has not yet been proven.
Future Therapies
Although many alternative therapies and interventions are available, few are supported by scientific studies. Lack of support for interventions: [4]
- Treatment approaches have little empirical support in quality-of-life contexts, and many programs focus on success measures that lack predictive validity and real-world relevance.
- Scientific evidence appears to matter less to service providers than program marketing, training availability, and parent requests.[5]
Although most alternative treatments, such as melatonin, have only mild adverse effects,[6] a 2008 study found that autistic boys on casein-free diets have significantly thinner bones,[7] and botched chelation therapy killed a five-year-old autistic boy in 2005.[8]
Approximately twelve research studies are published each week on autism therapies. Three major barriers inhibit transfer of this information from the laboratory to the child:
- Treatment providers do not routinely turn to treatments that have been validated scientifically.
- A large minority of patients (actually parents of patients) resist therapies that have been scientifically validated.
- Even scientifically validated therapies are not universally effective.[9]
References
- ↑ Oberman LM, Hubbard EM, McCleery JP, Altschuler EL, Ramachandran VS, Pineda JA., EEG evidence for mirror neuron dysfunction in autism spectral disorders, Brain Res Cogn Brain Res.; 24(2):190-8, 2005-06
- ↑ Mirella Dapretto, Understanding emotions in others: mirror neuron dysfunction in children with autism spectrum disorders, Nature Neuroscience, Vol. 9, No. 1, pp. 28-30, 2006-01
- ↑ Hadjikhani; et al. "Anatomical Differences in the Mirror Neuron System and Social Cognition Network in Autism". Cerebral Cortex. PMID 16306324.
- ↑ *Francis K (2005). "Autism interventions: a critical update" (PDF). Dev Med Child Neurol. 47 (7): 493–9. doi:10.1017/S0012162205000952. PMID 15991872.
- Rao PA, Beidel DC, Murray MJ (2008). "Social skills interventions for children with Asperger's syndrome or high-functioning autism: a review and recommendations". J Autism Dev Disord. 38 (2): 353–61. doi:10.1007/s10803-007-0402-4. PMID 17641962.
- Schechtman MA (2007). "Scientifically unsupported therapies in the treatment of young children with autism spectrum disorders" (PDF). Pediatr Ann. 36 (8): 497–8, 500–2, 504–5. PMID 17849608.
- ↑ Stahmer AC, Collings NM, Palinkas LA (2005). "Early intervention practices for children with autism: descriptions from community providers". Focus Autism Other Dev Disabl. 20 (2): 66–79. PMC 1350798. PMID 16467905.
- ↑ Angley M, Semple S, Hewton C, Paterson F, McKinnon R (2007). "Children and autism—part 2—management with complementary medicines and dietary interventions" (PDF). Aust Fam Physician. 36 (10): 827–30. PMID 17925903.
- ↑ Hediger ML, England LJ, Molloy CA, Yu KF, Manning-Courtney P, Mills JL (2008). "Reduced bone cortical thickness in boys with autism or autism spectrum disorder". J Autism Dev Disord. 38 (5): 848–56. doi:10.1007/s10803-007-0453-6. PMID 17879151. Lay summary – NIH News (2008-01-29).
- ↑ Brown MJ, Willis T, Omalu B, Leiker R (2006). "Deaths resulting from hypocalcemia after administration of edetate disodium: 2003–2005". Pediatrics. 118 (2): e534–6. doi:10.1542/peds.2006-0858. PMID 16882789.
- ↑ Bodfish JW (2004). "Treating the core features of autism: are we there yet?". Ment Retard Dev Disabil Res Rev. 10 (4): 318–26. doi:10.1002/mrdd.20045. PMID 15666340.