Autism: Neural Basis and Treatment Possibilities (Novartis by Novartis Foundation

By Novartis Foundation

This publication attracts jointly contributions from many of the major investigators within the box of autism to contemplate particular troublesome areas in present learn. every one contributor brings services from a unique box, delivering a balanced view of the entire spectrum of research of this ailment. It covers 4 major areas:

* dual and family members experiences point out that the heritability of the underlying legal responsibility to autism exceeds ninety% and element to a multifactorial causation, regarding a comparatively small variety of susceptibility genes. The publication discusses this factor intimately, in addition to the matter of why a few extra indicators are linked to autism whereas others are not.

* New innovations can be found for studying the neurobiology of autism. The publication comprises effects from imaging reports displaying the contributions of alternative mind areas to autism. It contains neuropathological information and examines the neuropharmacology of autism.

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Additional resources for Autism: Neural Basis and Treatment Possibilities (Novartis Foundation Symposia)

Sample text

We do not know how well the ADI discriminates autism from PDD-NOS, but we do know that the ADOS doesn’t make this discrimination well on an individual basis (Lord et al 2000). The ADOS tends to be over-inclusive for autism for children with clinical reports of atypical autism or PDD-NOS, and also misses some of the highest-functioning subjects. This is what Bertrand et al got: a higher prevalence of autism than the other studies and a lower prevalence of ASDs than British studies. Dawson: I wanted to comment about something that was mentioned earlier about early development.

E. the underlying mechanisms are considered unrelated to those causing autism speci¢c de¢cits. If these properties are emergent, however, then as milder phenotypes are not associated with mental handicap or epilepsy, the biochemical mechanisms seem unlikely to a¡ect the fundamental properties of neurons. Rather handicap and epilepsy presumably emerge because more severe expression involves increasingly abnormal interactions between neurons. Indeed over the last few years it has been appreciated that autism is associated with other nonlocalized neurodevelopmental abnormalities, including increased head circumference (¢rst noted by Kanner in 1943), increased brain volume and BROADER PHENOTYPE 33 weight (Piven et al 1995, Bailey et al 1998a) and developmental cortical abnormalities (Bailey et al 1998a).

There are methodologically sound epidemiological approaches that would tell us whether in a particular geographical location children are exposed to these kinds of events. Do we ¢nd increases in prevalence there? It is not answering the same question, but I do think we have more hope for studying the other side of the question of what the factors might be. If we ¢nd that all the hypothesized factors we can imagine are negative, this is an important piece of circumstantial evidence. Fombonne: You would need a strong hypothesis to start with.

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