Summary: New research shows that different genetic forms of autism may produce a shared brain activity pattern, revealing a potential common neural signature despite distinct genetic origins. Using brain-wide recordings in preclinical models, scientists observed that autism-linked mutations affected how expectations are updated during decision-making.
These models relied more heavily on frontal brain regions and less on sensory input, struggling to distinguish between predictable and unpredictable stimuli. The findings offer a promising bridge between genetic variation and behavioral traits in autism, opening new paths for targeted research.
Key Facts:
- Shared Brain Signature: Distinct autism-linked genes produce similar patterns of brain activity.
- Sensory Processing Differences: Autism models show impaired flexibility in updating expectations from sensory input.
- Frontal Dominance: Mutant models relied more on frontal brain regions, less on sensory areas during decision-making.
Source: University of Minnesota
New research from the University of Minnesota Medical School suggests that different genetic forms of autism may lead to similar patterns in brain activity and behavior.
The findings were recently published in Nature Neuroscience.
Using brain-recording technology, the research team observed neurons across the entire brain to explore whether different genetic forms of autism share patterns and establish commonalities in neural responses.
They found that, despite genetic differences, various forms may show a similar unique pattern of brain activity — also known as a brain signature.
“We hope this research will serve as a stepping stone linking genetic differences and behavioral atypicalities,” said Jean-Paul Noel, PhD, an assistant professor at the University of Minnesota Medical School.
The study found that preclinical models with autism-linked genetic mutations struggled to adjust their expectations —or their predicted state of the world in the immediate future — based on new information when making decisions.
Unlike typical models that could update their expectations more flexibly, they relied more heavily on the front part of the brain and less on sensory areas.
As a result, their brains focused more on long-term expectation differences, but their sensory systems had trouble distinguishing between predictable and unpredictable sensory stimuli.
The particular circuit this research uncovered appears to drive behavioral anomalies in all three preclinical models of autism tested. This feedback projection from frontal areas to visual cortex will be studied in more detail in subsequent projects.
Funding: This research was supported by grants from the Wellcome Trust, Simons Foundation, National Institutes of Health [grant R00NS128075], a Simons Foundation Autism Research Initiative Pilot Grant, the University of Minnesota Clinical and Translational Science Institute and a Sloan Research fellowship.
About this genetics and Autism research news
Author: Alexandra Smith
Source: University of Minnesota
Contact: Alexandra Smith – University of Minnesota
Image: The image is credited to Neuroscience News
Original Research: Closed access.
“A common computational and neural anomaly across mouse models of autism” by Jean-Paul Noel et al. Nature Neuroscience
Abstract
A common computational and neural anomaly across mouse models of autism
Computational psychiatry studies suggest that individuals with autism spectrum disorder (ASD) inflexibly update their expectations.
Here we leveraged high-yield rodent psychophysics, extensive behavioral modeling and brain-wide single-cell extracellular recordings to assess whether mice with different genetic perturbations associated with ASD show this same computational anomaly, and if so, what neurophysiological features are shared across genotypes.
Mice harboring mutations in Fmr1, Cntnap2 or Shank3B show a blunted update of priors during decision-making.
Compared with mice that flexibly updated their priors, inflexible updating of priors was associated with a shift in the weighting of prior encoding from sensory to frontal cortices.
Furthermore, frontal areas in mouse models of ASD showed more units encoding deviations from the animals’ long-run prior, and sensory responses did not differentiate between expected and unexpected observations.
These findings suggest that distinct genetic instantiations of ASD may yield common neurophysiological and behavioral phenotypes.
