Functional connectivity in the brain refers to the synchronization of neuronal circuits to transfer information within and between the circuits. Long-range cortical functional connectivity, which links distant areas in the cortex, is often weaker in people with autism spectrum disorders than in controls. It is generally thought, however, that local functional connectivity is stronger in people with the disorder than in controls.
Using fMRI in typically developing children, Vinod Menon finds one’s mother’s voice activates a network of brain regions predictive of a child’s social communication skills.
Neuroimaging studies have described altered structural and functional connectivity across brain regions of individuals with autism spectrum disorder (ASD). These findings have led to the hypothesis that altered brain connectivity may provide a key pathophysiological contribution in ASD. However the neurobiological determinants and significance of these findings remain unclear.
Human brain function is the result of a highly organized network of connections linking multiple areas across the brain. A popular theory to explain autism is that genetic variants interact with environmental factors and lead to impaired or dysfunctional communication between these unique brain areas. However, the genetic and neurobiological determinants of the connectivity impairments observed in autism are largely unknown.
Many children with autism have unusually high numbers of synapses, or connections between neurons, particularly in the cortex, which may result from overgrowth and a disruption of neuronal pruning during childhood. Pruning and reshaping of neurons pares down the number of synapses in the brain while eliminating inappropriate synapses that lead to over-connectivity between brain regions, and possibly inappropriate learning, behavior and seizures. David Sulzer and his colleagues at Columbia University hypothesize that autism-associated mutations in the tuberous sclerosis gene, TSC, can cause over-connectivity when the target of TSC, the mTOR pathway, interferes with normal neuronal pruning.
Cognitive and behavioral impairments in autism spectrum disorders are thought to result from changes in the structure and function of brain circuits. Disruption of the balance between excitation and inhibition in the neocortex has been proposed as a possible mechanism. This type of imbalance could lead to altered neuronal network connections that give rise to dramatic changes in the way the brain processes information and regulates behavior.
Susan Bookheimer and colleagues show that the degree of sensory overresponsivity in individuals with autism may be driven by distinct patterns of connectivity between the prefrontal cortex and amygdala.
James Ellis and colleagues used a sparse co-culture system for iPSC-derived cortical neurons to assess neuronal connectivity, demonstrating increased connectivity in SHANK2-mediated ASD.
Daniel Geschwind and colleagues showed that Cntnap2 knockout mice exhibit alterations in brain-wide connectivity related to social behaviors and that oxytocin within the nucleus accumbens regulates changes in connectivity.
Alessandro Gozzi and colleagues found that Shank3-deficient mice have disrupted frontocortical functional connectivity, which is associated with impaired communication and social behaviors.
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