How do we connect the dots of connectivity?

Growing evidence suggests that abnormal connectivity in the brain underlies autism, but conflicting interpretations persist about where and how the dysfunction occurs. How do we investigate the underlying mechanisms of this theory?

By Greg Boustead
22 March 2013 | 2 min read
This article is more than five years old.
Neuroscience—and science in general—is constantly evolving, so older articles may contain information or theories that have been reevaluated since their original publication date.


Special Report: Connectivity


This is one of a series of articles exploring brain connectivity in autism.
Read more »


Today we present our special report on connectivity, a collection of guest blogs and other features exploring the theory that abnormal neural connectivity underlies autism.

Check out the complete package here »

The collection provides a snapshot of the existing data supporting the theory, as well as some open debates and technological challenges.

Critically, there remain many open research questions, several of which came up in conversations with researchers and with our science team during the process of putting this package together.

What do you think?

  • Marcel Adam Just and Timothy Keller suggest in their viewpoint that rather than a global reduction of connectivity, connectivity in autism is reduced specifically between the frontal cortex and other brain regions.
  • What underlying mechanisms might result in that pattern?
  • Could altered connectivity during development drive some of the observed anomalies in autism, such as a large head or altered trajectory of brain growth? Or are these deficits themselves a root cause of reduced connectivity?

Given the diversity of risk genes that are implicated in autism, and the variability in symptoms from person to person, how likely is it that reduced connectivity is a convergent hallmark of the disorder?

Share your thoughts in the comments section below.