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Review
. 2006 Jun 28;26(26):6897-906.
doi: 10.1523/JNEUROSCI.1712-06.2006.

The developmental neurobiology of autism spectrum disorder

Emanuel DiCicco-Bloom  1 , Catherine Lord, Lonnie Zwaigenbaum, Eric Courchesne, Stephen R Dager, Christoph Schmitz, Robert T Schultz, Jacqueline Crawley, Larry J Young
Affiliations
Review

The developmental neurobiology of autism spectrum disorder

Emanuel DiCicco-Bloom et al. J Neurosci. .
No abstract available

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Figures

Figure 1.
Figure 1.
Functional MRI abnormalities observed in ASD. A, These coronal MRI images show the cerebral hemispheres above, the cerebellum below, and a circle over the fusiform gyrus of the temporal lobe. The examples illustrate the frequent finding of hypoactivation of the fusiform gyrus to faces in an adolescent male with ASD (right) compared with an age- and IQ-matched healthy control male (left). The red/yellow signal shows brain areas that are significantly more active during perception of faces; signals in blue show areas more active during perception of nonface objects. Note the lack of face activation in the boy with ASD but average levels of nonface object activation. B, Schematic diagrams of the brain from lateral and medial orientations illustrating the broader array of brain areas found to be hypoactive in ASD during a variety of cognitive and perceptual tasks that are explicitly social in nature. Some evidence suggests that these areas are linked to form a “social brain” network. IFG, Inferior frontal gyrus (hypoactive during facial expression imitation); pSTS, posterior superior temporal sulcus (hypoactive during perception of facial expressions and eye gaze tasks); SFG, superior frontal gyrus (hypoactive during theory of mind tasks, i.e., when taking another person’s perspective); A, amygdala (hypoactive during a variety of social tasks); FG, fusiform gyrus, also known as the fusiform face area (hypoactive during perception of personal identity) (Schultz, 2005; Schultz and Robins, 2005).
Figure 2.
Figure 2.
Genomic structure and association results of the ENGRAILED 2 gene. EN2 is encoded by two exons separated by a single intron in 8.1 kb. Eighteen polymorphisms within EN2 have been tested for association with ASD, and two intronic SNPs (rs1861972 and rs1861973) have consistently displayed significant results. Rs1861972 is an A/G polymorphism, and rs1861973 is a C/T polymorphism. Significant association for the A allele of rs1861972 and the C allele of rs1861973, both individually and as a haplotype, has been observed in three separate datasets, providing genetic evidence that EN2 is likely to be an ASD susceptibility locus (Gharani et al., 2004; Benayed et al., 2005) [ASD (Mendelian Inheritance in Man MIM 608636); EN2 (MIM 131310)].
Figure 3.
Figure 3.
Methods for phenotyping animal social behavior. A, The subject mouse is placed in the center chamber and has a choice between spending time exploring a novel object, the wire pencil cup in the left compartment, or spending time with a novel mouse, in the right compartment. Photocells across the openings detect the movements between compartments. Software scores the time in each compartment and number of compartment entries. Normal mice of most inbred strains spend more time in the compartment containing the stranger mouse. B, Social interaction between the subject mouse and the unfamiliar conspecific is scored by an observer with a stopwatch. Containing the stranger mouse in the wire cup ensures that all social approach is initiated by the subject mouse and is investigatory only, with no opportunity for sexual or aggressive interactions (Crawley, 2000, 2004).
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