The brain's ability to process information crucially relies on connectivity. Understanding how the brain processes complex information and how such abilities are disrupted in individuals with neuropsychological disorders will require an improved understanding of brain connectivity. Autism is an intriguingly complex neurodevelopmental disorder with multidimensional symptoms and cognitive characteristics. A biological origin for autism spectrum disorders (ASD) had been proposed even in the earliest published accounts (Kanner, 1943; Asperger, 1944). Despite decades of research, a focal neurobiological marker for autism has been elusive. Nevertheless, disruptions in interregional and functional and anatomical connectivity have been a hallmark of neural functioning in ASD. Theoretical accounts of connectivity perceive ASD as a cognitive and neurobiological disorder associated with altered functioning of integrative circuitry. Neuroimaging studies have reported disruptions in functional connectivity (synchronization of activated brain areas) during cognitive tasks and during task-free resting states. While these insights are valuable, they do not address the time-lagged causality and directionality of such correlations. Despite the general promise of the connectivity account of ASD, inconsistencies and methodological differences among studies call for more thorough investigations. A comprehensive neurological account of ASD should incorporate functional, effective, and anatomical connectivity measures and test the diagnostic utility of such measures. In addition, questions pertaining to how cognitive and behavioral intervention can target connection abnormalities in ASD should be addressed. This research topic of the Frontiers in Human Neuroscience will address “Brain Connectivity in Autism” primarily from cognitive neuroscience and neuroimaging perspectives.
Specifically with respect to the wealth of neuroimaging findings, fundamental questions still await definitive answers. Among these are:
• How can the inconsistencies in the fcMRI literature – with abundant evidence of underconnectivity in many functional networks contrasting with some reports of overconnectivity in ASD – be explained and reconciled?
• How do findings for low temporal frequency bands from fcMRI relate to those for higher frequencies, as detected by EEG and MEG?
• What are the underlying pathological changes suggested by DTI findings of reduced fractional anisotropy or increased mean and radial diffusion?
• How does evidence of white matter compromise and abnormal functional connectivity in children and adults relate to evidence of early brain overgrowth in infants that develop ASD?
• What are the links between abnormalities of functional and anatomical connectivity and those of cortical organization, e.g., those affecting cytoarchitecture or regional cortical thickness?
• How can techniques that are not typically applied in connectivity studies (e.g., TMS, MR spectroscopy) contribute to the understanding of connectivity in ASD?
• How do imaging findings inform us about the causation of sociocommunicative and other impairments in ASD? How can we determine whether they provide developmental explanations or simply reflect atypical social interaction in children with ASD?
We welcome contributions addressing one (or several) of the questions above or any other relevant questions related to network connectivity in ASD. Specifically, we welcome not only authors with a track record in ASD connectivity research, but also those in fields not conventionally considered to be related to connectivity (e.g., postmortem cytoarchitectonics, brain volumetrics, computational modeling), who may add valuable ‘outside-the-box’ contributions. The main goal of this venture is to search for a comprehensive and cohesive framework for better conceptualization of connection abno
The brain's ability to process information crucially relies on connectivity. Understanding how the brain processes complex information and how such abilities are disrupted in individuals with neuropsychological disorders will require an improved understanding of brain connectivity. Autism is an intriguingly complex neurodevelopmental disorder with multidimensional symptoms and cognitive characteristics. A biological origin for autism spectrum disorders (ASD) had been proposed even in the earliest published accounts (Kanner, 1943; Asperger, 1944). Despite decades of research, a focal neurobiological marker for autism has been elusive. Nevertheless, disruptions in interregional and functional and anatomical connectivity have been a hallmark of neural functioning in ASD. Theoretical accounts of connectivity perceive ASD as a cognitive and neurobiological disorder associated with altered functioning of integrative circuitry. Neuroimaging studies have reported disruptions in functional connectivity (synchronization of activated brain areas) during cognitive tasks and during task-free resting states. While these insights are valuable, they do not address the time-lagged causality and directionality of such correlations. Despite the general promise of the connectivity account of ASD, inconsistencies and methodological differences among studies call for more thorough investigations. A comprehensive neurological account of ASD should incorporate functional, effective, and anatomical connectivity measures and test the diagnostic utility of such measures. In addition, questions pertaining to how cognitive and behavioral intervention can target connection abnormalities in ASD should be addressed. This research topic of the Frontiers in Human Neuroscience will address “Brain Connectivity in Autism” primarily from cognitive neuroscience and neuroimaging perspectives.
Specifically with respect to the wealth of neuroimaging findings, fundamental questions still await definitive answers. Among these are:
• How can the inconsistencies in the fcMRI literature – with abundant evidence of underconnectivity in many functional networks contrasting with some reports of overconnectivity in ASD – be explained and reconciled?
• How do findings for low temporal frequency bands from fcMRI relate to those for higher frequencies, as detected by EEG and MEG?
• What are the underlying pathological changes suggested by DTI findings of reduced fractional anisotropy or increased mean and radial diffusion?
• How does evidence of white matter compromise and abnormal functional connectivity in children and adults relate to evidence of early brain overgrowth in infants that develop ASD?
• What are the links between abnormalities of functional and anatomical connectivity and those of cortical organization, e.g., those affecting cytoarchitecture or regional cortical thickness?
• How can techniques that are not typically applied in connectivity studies (e.g., TMS, MR spectroscopy) contribute to the understanding of connectivity in ASD?
• How do imaging findings inform us about the causation of sociocommunicative and other impairments in ASD? How can we determine whether they provide developmental explanations or simply reflect atypical social interaction in children with ASD?
We welcome contributions addressing one (or several) of the questions above or any other relevant questions related to network connectivity in ASD. Specifically, we welcome not only authors with a track record in ASD connectivity research, but also those in fields not conventionally considered to be related to connectivity (e.g., postmortem cytoarchitectonics, brain volumetrics, computational modeling), who may add valuable ‘outside-the-box’ contributions. The main goal of this venture is to search for a comprehensive and cohesive framework for better conceptualization of connection abno