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And that investment has paid scientific dividends, above all the uncovering of genetic clues to underlying mechanisms for the disorder. But, as discussed in this special issue and in a web collection of content published this week in other Nature journals see nature. Context, as always, is important. First, the object of study: it is clear that the diagnostic criteria for autism need to be refined and expanded, and that there is a spectrum of autistic disorders. Second, although most parents struggling with children with autism would jump at the chance to mitigate or cure the symptoms, it is not appropriate to think of autism solely as a disorder needing treatment.
And that perspective plays into a range of ethical implications for the pursuit of biomarkers for the condition P. Nature Rev. Everyone agrees that autism stems from a disruption of brain development caused by a combination of genes and environment. Since the s, it has been known from studies of twins that there is a high, but not complete, degree of heritability.
In recent years, well-funded and coordinated efforts, coupled with advances in technology, have led to large-scale studies of unprecedented statistical power, producing impressive data on the genetics of the condition. But those data have confirmed only that the answer is elusively complicated. An emerging story is that the culprits could include any one of many extraordinarily rare genetic variations, and that a systems approach will be important in understanding regulatory hubs, for example M.
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State and P. Levitt Nature Neurosci. Nonetheless, progress is being made in tracking the neuro biological effects of these genetic variations. Recently, mice carrying mutations in candidate genes have been produced, and have been found to show behaviours reminiscent of autism — such as a lack of interest in socializing with other mice, repetitive grooming and anxiety. These mice all have alterations in brain structure and function, and will undoubtedly be useful for testing hypotheses about the relationship between various brain circuits and autism-associated behaviour see, for example, J.
Neul Nature Med. Along with these mice, cellular models derived from patients carrying certain mutations also hold promise for testing molecular hypotheses and therapies. Encouraging as these efforts are, they cover just half of the gene—environment equation and thus will at best only ever yield part of the solution. It is widely agreed that environmental factors, through direct neurobiological mechanisms or interactions with genes, could interfere with neural development to cause autism.
Many factors have been proposed, including maternal infection during pregnancy. But none of these candidates has yet been convincingly established, nor have their biological links to autism been tested mechanistically. Clearly, nailing down a given influencing factor from our incredibly complex environment is no trivial task, possibly harder than identifying variation in the genome.
It will take very large and expensive long-term studies just to narrow down the possibilities.
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