The name is absent

Autism prodrome 43 of 89

The causes of autism are still largely unknown but there are several lines of
evidence to support the predominant effect of genetic factors. Many genetic factors
are probably involved in the etiology of ASDs and various genetic markers may be
involved with various developmental trajectories and prodromes of the many ASDs.
Twin studies show concordance rates between monozygotic twins of 70-90%,
whereas dizygotic twins show 0-10% concordance (Bailey et al., 1995; Folstein &
Rutter, 1977; Hurley, Losh, Parlier, Reznick, & Piven, 2007; Steffenburg et al.,
1989). The prevalence of autism in siblings of autistic individuals is ∙ 5% (Rutter,
Silberg, O'Connor, & Simonoff, 1999), considerably higher than the population
prevalence of 0.37%. In addition, as shown below, a growing body of literature
demonstrates that genetic variations in any of several genes can dramatically
increase disease risk and thus constitute an etiological factor for ASDs. It is
noteworthy that in some of the few high risk sibling studies reporting outcomes
through to the age of 3 years recurrence rates appear to be considerably higher, both
for ASD outcomes and for other developmental delays. Yet it is likely that biases
operate in such studies including enrolling children who already show worrying
some signs, particularly in studies where siblings are recruited after 6 months of age
(e.g. Landa et al., 2007; Zwaigenbaum et al., 2005).

Although the allelic architecture of autism will probably be revealed only from
a large amount of empirical data, current studies indicate that a combination of
common and rare variants, including de novo mutations (spontaneous mutations as
opposed to inherited variations), might account for ASD. Until now, most of the
genetic variations that were found to be associated with ASD are rare or de novo
mutations, however, none of these known causes accounts for more than 1-2% of
cases. Since ASD is an early onset disease with an impact on reproductive fitness, it is

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