Summary: New research indicates that despite having unique genetic roots, unique genetic forms of autism may produce a common brain activity pattern, indicating a possible common neural signature. Researchers found that autism-linked variants had an impact on how expectations were updated during decision-making by using brain-wide recordings of experimental models.
These models struggled to distinguish between repetitive and uncertain stimuli because they more heavily relied on front brain areas and less on sensory input. The findings provide a promising link between dementia behavioral traits and genetic variation, opening up new avenues for research.
Important Information
- Similar Brain Activity Patterns are produced by different autism-linked genes.
- Sensory Processing Distinctions: Autism models show decreased flexibility when updating expectations based on sensory input.
- Front Dominance: Mutated models relied more on front brain regions and less on sensory areas for decision-making.
University of Minnesota
New findings from the University of Minnesota Medical School point to the possibility that unique genetic variations of dementia may cause brain activity and behavior to be similar.
The results were just published in Nature Science.  ,
The analysis team used brain-recording technology to observe neurons across the entire brain to determine whether various biological forms of dementia discuss patterns and create commonalities in neurological responses.
Despite genetic differences, they discovered that different forms may exhibit a similar distinct pattern of brain activity, also known as a mental personal.
Jean-Paul Noel, PhD, an associate professor at the University of Minnesota Medical School, said,” We hope this research may serve as a stepping stone linking biological differences and behavioural atypicalities.”  ,
The study found that experimental models with autism-linked biological abnormalities struggled to adjust their expectations based on fresh data when making decisions, especially regarding the world’s immediate future.
They relied more heavily on the front part of the brain and less on visual places, in contrast to standard models, who could release their expectations more freely.
In consequence, their brains concentrated more on long-term desire differences, but their sensory systems struggled to distinguish between repetitive and uncertain visual stimuli.  ,
In all three preliminary autism models tested, the specific circuit that this study discovered appears to be responsible for behavioral oddities. In upcoming projects, more in-depth analysis of this feedback projection from lateral areas to the visual cortex may be conducted.
Funding: This study was supported by offers from the University of Minnesota, the Clinical and Translational Science Institute, the Wellcome Trust, the Simons Foundation, and the National Institutes of Health [grant R00NS128075], as well as a Sloan Research Fellowship.  ,
About this news article on dementia and genetics
Author: Alexandra Smith
Source: University of Minnesota
Contact: Alexandra Smith – University of Minnesota
Image: The image is credited to Neuroscience News
Original Research: Private entry.
By Jean-Paul Noel and albert.,” A common computing and neurological anomaly across rat models of adhd.” Science of the natural world
Abstract
A typical computing and neurological anomaly in autism mouse models
According to computational psychiatry research, people with autism spectrum disorder ( ASD ) inflexibly update their expectations.
To determine whether mice with unique genetic perturbations associated with ASD display this same mathematical anomaly, we used high-yield mouse psychophysics, intensive behavior modeling, and brain-wide single-cell external recordings to test whether this pattern is present in different genotypes and whether or not these neurophysiological features are shared across genotypes.
Mice with mutations in , Fmr1,  , Cntnap2 , or Shank3B  exhibit blunted update of priors during decision-making.
Inflexible updating of priors was associated with a shift in the weighting of prior encoding from sensory to frontal cortices in mice that flexibly updated their priors.
Additionally, frontal areas in ASD mouse models showed more units encoding deviations from the animals ‘ long-run prior, and sensory responses did not distinguish between expected and unanticipated observations.
These findings point to the possibility that different ASD genetic instantiations may result in similar neurophysiological and behavioral phenotypes.
