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fMRI findings may enable researchers to further the understanding of the neural systems underlying autism.
With use of fMRI, researchers have identified a pattern of brain activity that may characterize a child’s genetic vulnerability to develop autism spectrum disorder (ASD), according to a study in the November 15 online Proceedings of the National Academy of Sciences.
The investigators administered an fMRI scan to a group of children, ages 4 to 17, who viewed coherent and scrambled point-light animations of biologic motion in a blocked design. Twenty-five children had ASD, 20 were unaffected siblings of children with ASD, and 17 were typically developing children. By comparing the activation to biologic motion versus that of scrambled motion in the subjects, the investigators observed three types of neural signatures, noted Martha D. Kaiser, PhD, of the Yale School of Medicine in New Haven, Connecticut, and colleagues.
The first type, state activity, is related to the state of having ASD that characterizes the nature of disruption in brain circuitry. The second, trait activity, reflects shared areas of dysfunction in unaffected siblings and children with ASD, thereby providing a possible neuroendophenotype to help efforts in linking genomic complexity and disorder heterogeneity, according to Dr. Kaiser. The third neural signature, compensatory activity, is unique to unaffected siblings, suggesting a neural system-level mechanism by which they may compensate for an increased genetic risk for developing ASD.
“The distinct brain responses to biologic motion exhibited by typically developing children and unaffected siblings are striking given the identical behavioral profile of these two groups,” the researchers reported. “These findings offer far-reaching implications for our understanding of the neural systems underlying autism.
“This fMRI study features the youngest groups of children with and without ASD studied to date, offering a substantial contribution to characterizing early developmental stages of disruptions in the neural systems associated with ASD,” Dr. Kaiser and colleagues concluded. “These disruptions in brain function may arise from various genetic and molecular etiologies and are further transformed across development by the experiences and activity of the individual in the world. Notably, the presence of state, trait, and compensatory activity, elicited by the viewing of socially relevant biologic motion, emphasizes the importance of brain mechanisms in social perception as well as the dysfunction of these mechanisms in this neurodevelopmental disorder.”
Suggested Reading
Kaiser MD, Hudac CM, Shultz S, et al. Neural signatures of autism. Proc Natl Acad Sci USA. 2010 Nov 15; [Epub ahead of print].
fMRI findings may enable researchers to further the understanding of the neural systems underlying autism.
With use of fMRI, researchers have identified a pattern of brain activity that may characterize a child’s genetic vulnerability to develop autism spectrum disorder (ASD), according to a study in the November 15 online Proceedings of the National Academy of Sciences.
The investigators administered an fMRI scan to a group of children, ages 4 to 17, who viewed coherent and scrambled point-light animations of biologic motion in a blocked design. Twenty-five children had ASD, 20 were unaffected siblings of children with ASD, and 17 were typically developing children. By comparing the activation to biologic motion versus that of scrambled motion in the subjects, the investigators observed three types of neural signatures, noted Martha D. Kaiser, PhD, of the Yale School of Medicine in New Haven, Connecticut, and colleagues.
The first type, state activity, is related to the state of having ASD that characterizes the nature of disruption in brain circuitry. The second, trait activity, reflects shared areas of dysfunction in unaffected siblings and children with ASD, thereby providing a possible neuroendophenotype to help efforts in linking genomic complexity and disorder heterogeneity, according to Dr. Kaiser. The third neural signature, compensatory activity, is unique to unaffected siblings, suggesting a neural system-level mechanism by which they may compensate for an increased genetic risk for developing ASD.
“The distinct brain responses to biologic motion exhibited by typically developing children and unaffected siblings are striking given the identical behavioral profile of these two groups,” the researchers reported. “These findings offer far-reaching implications for our understanding of the neural systems underlying autism.
“This fMRI study features the youngest groups of children with and without ASD studied to date, offering a substantial contribution to characterizing early developmental stages of disruptions in the neural systems associated with ASD,” Dr. Kaiser and colleagues concluded. “These disruptions in brain function may arise from various genetic and molecular etiologies and are further transformed across development by the experiences and activity of the individual in the world. Notably, the presence of state, trait, and compensatory activity, elicited by the viewing of socially relevant biologic motion, emphasizes the importance of brain mechanisms in social perception as well as the dysfunction of these mechanisms in this neurodevelopmental disorder.”
fMRI findings may enable researchers to further the understanding of the neural systems underlying autism.
With use of fMRI, researchers have identified a pattern of brain activity that may characterize a child’s genetic vulnerability to develop autism spectrum disorder (ASD), according to a study in the November 15 online Proceedings of the National Academy of Sciences.
The investigators administered an fMRI scan to a group of children, ages 4 to 17, who viewed coherent and scrambled point-light animations of biologic motion in a blocked design. Twenty-five children had ASD, 20 were unaffected siblings of children with ASD, and 17 were typically developing children. By comparing the activation to biologic motion versus that of scrambled motion in the subjects, the investigators observed three types of neural signatures, noted Martha D. Kaiser, PhD, of the Yale School of Medicine in New Haven, Connecticut, and colleagues.
The first type, state activity, is related to the state of having ASD that characterizes the nature of disruption in brain circuitry. The second, trait activity, reflects shared areas of dysfunction in unaffected siblings and children with ASD, thereby providing a possible neuroendophenotype to help efforts in linking genomic complexity and disorder heterogeneity, according to Dr. Kaiser. The third neural signature, compensatory activity, is unique to unaffected siblings, suggesting a neural system-level mechanism by which they may compensate for an increased genetic risk for developing ASD.
“The distinct brain responses to biologic motion exhibited by typically developing children and unaffected siblings are striking given the identical behavioral profile of these two groups,” the researchers reported. “These findings offer far-reaching implications for our understanding of the neural systems underlying autism.
“This fMRI study features the youngest groups of children with and without ASD studied to date, offering a substantial contribution to characterizing early developmental stages of disruptions in the neural systems associated with ASD,” Dr. Kaiser and colleagues concluded. “These disruptions in brain function may arise from various genetic and molecular etiologies and are further transformed across development by the experiences and activity of the individual in the world. Notably, the presence of state, trait, and compensatory activity, elicited by the viewing of socially relevant biologic motion, emphasizes the importance of brain mechanisms in social perception as well as the dysfunction of these mechanisms in this neurodevelopmental disorder.”
Suggested Reading
Kaiser MD, Hudac CM, Shultz S, et al. Neural signatures of autism. Proc Natl Acad Sci USA. 2010 Nov 15; [Epub ahead of print].
Suggested Reading
Kaiser MD, Hudac CM, Shultz S, et al. Neural signatures of autism. Proc Natl Acad Sci USA. 2010 Nov 15; [Epub ahead of print].