The Role Of Evolutionary Genomics In The Development Of Autism

[Odin2005]

http://www.sciencedaily.com/releases/2006/03/060322182837.htm

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(removed the first paragraph to conform to the 4-paragraph rule)

In an article to be published in a forthcoming issue of Journal of Evolutionary Biology, Dr Christopher Badcock and Professor Bernard Crespi explore the 'imprinted brain hypothesis' to explain the cause and effect of autism and autistic syndromes such as Asperger's syndrome, highlighted by the book The Curious Incident of the Dog in the Night-Time, which involves selective disruption of social behaviour that makes individuals more self-focussed whilst enhancing skills related to mechanistic cognition.

The 'imprinted brain hypothesis' suggests that competition between maternally and paternally expressed genes leads to conflicts within the autistic individual which could result in an imbalance in the brain's development. This is supported by the fact that there is known to be a strong genomic imprinting component to the genetic and developmental mechanisms of autism and autistic syndromes.

Professor Bernard Crespi from Simon Fraser University, Canada explains: "The imprinted brain hypothesis underscores the viewpoint that the autism spectrum represents human cognitive diversity rather than simply disorder or disability. Indeed, individuals at the highest-functioning end of this spectrum may have driven the development of science, engineering and the arts through mechanistic brilliance coupled with perseverant obsession."

The core behavioural features of autism such as self-focussed behaviour, altered social interactions and language and enhanced spatial and mechanistic cognition and abilities -- as well as the degree to which the brain functions and structures are altered -- also supports this hypothesis.
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More proof that Austism is genetic.

[back2basics909]

1. Autism..

..is a range of conditions, they call it a spectrum. Aspergers has always seemed very different, and it does appear this research is talk about Aspergers and maybe some other forms.

I think there is a little more to the more severe forms, and also the regresive forms. NOt sure what, i know it's not MMR or Thermasal (directly) althugh they may play a small role due to an auto-immune responce making things worse, after the childs immune system is weakened by a genetic weakness issue.

This is also just a hypothasis, not a tested theory.

We should be carefull, at this early stage, to think all forms of Autism have the same cause.

[depakid]

2. Genetic predispositions

don't mean that an individual will necessarily develop the neurological condition. Bipolar disorder (or it's affective spectrum) is also genetic- actual loci have been found- but twin studies show clearly that environmental factors that come into play.

I suspect the same sorts of mechanisms apply to the autistic spectrum. Could be some of these occur in utero (e.g., the Barker hypothesis) or are related to exposures during neurological window periods.

[Celebration]

3. autism is genetic AND

I was wondering what this person's explanation was for the increased numbers of autistic children, and found the whole study here--

http://www.blackwell-synergy.com/doi/full/10.1111/j.1420-9101.2006.01091.x?cookieSet=1

They certainly don't think it is *only* genetic--

Several lines of evidence implicate dysregulated methylation, and imprinting effects, in environmental determinants on autism. First, valproic acid induces autism when administered in early foetal development (Ingram et al., 2000b; Chudley, 2004; Schneider & Przewlocki, 2005), apparently via its role as a specific inhibitor of histone deacetylase activity, which reduces methylation of promotor regions (Detich et al., 2003). Experiments with mice indicate that effects of valproic acid on genomically imprinted genes contribute to its neurological effects (Beck, 2001), which include abnormalities in serotoninergic neurone development and hyperserotonaemia (Miyazaki et al., 2005). Thalidomide, which similarly leads to autism via perturbation of early brain development, exerts similar effects on the serotoninergic system (Narita et al., 2002; Miyazaki et al., 2005).

Second, impaired methionine metabolism, caused by heavy metals, thimerosal and other agents, and mediated by genetic factors such as propensity to autoimmune disease (Hornig et al., 2004), abnormal metal metabolism (Serajee et al., 2004), or adenosine deaminase activity, may cause dysregulated methylation and contribute to autism (Waly et al., 2004).

Third, autism increases with paternal (and maternal) age (Gillberg, 1980), and assisted reproduction via intracytoplasmic sperm injection (ICSI) may increase the risk for syndromes of dysregulated imprinting, including Angelman and Beckwith-Weideman (Paoloni-Giacobino & Chaillet, 2004; Waterland & Jirtle, 2004; Maher, 2005). Both paternal age and ICSI are expected to contribute to methylated-gene defects, which may include effects on brain-imprinted genes (Waterland & Jirtle, 2004; Malaspina et al., 2005).

Finally, James et al. (2004) demonstrated impaired methylation capacity in children with autism; altered methylation, and its effects on imprinted gene expression, can persist through development (Waterland & Jirtle, 2004). Monozygotic twins have also recently been demonstrated to diverge in their patterns of gene methylation starting in early development, which may contribute to their divergence in the expression of cognitive disorders (Petronis et al., 2003; Fraga et al., 2005; Wong et al., 2005).