“This is a long one… but I hope something here is useful. My frustration over my struggle to hold a job is still a big part of my life. But I hope I’m moving toward figuring out what will be sustainable. Unfortunately, being either under or unemployed is pretty standard for autistic women, so I feel the struggle and have so much compassion for anyone who is going through the same thing.”
A new study has identified distinct neural and behavioural characteristics in autism that a simple computational principle can explain. This research focuses on the “dynamic range” of neurons, which indicates how gradually or sharply they respond to stimuli. The findings suggest that individuals with autism spectrum disorder exhibit an increased dynamic range in their neuronal responses. As a result, they tend to have more detailed responses that are slower to adapt to changes. This study challenges previous views of autism as merely a “broken cog in the machine” and offers a more nuanced understanding of the computational foundations of autism.
Researchers Dr Yuval Hart and Oded Wertheimer from the Psychology Department and the Edmond and Lily Safra Center for Brain Science (ELSC) at the Hebrew University of Jerusalem have developed a new computational model to explain the neural and behavioural differences associated with autism. This model provides new insights into information processing in the brains of individuals with autism, paving the way for future research and deeper understanding.
Autism is known to present unique neural and behavioural characteristics compared to neurotypical individuals, but the underlying computational mechanisms remain complex and multifaceted. The model proposed by Dr Hart and Wertheimer centres around the concept of “dynamic range” within neuronal populations. Dynamic range refers to signals for which neurons elicit discernible responses. In simpler terms, it reflects how gradually or sharply neurons respond to stimuli – a more gradual response entails an increased dynamic range.
“Our model suggests that autism spectrum disorder is not a `broken cog in the machine`, but rather a spectrum of points on the computational tradeoff line between accurate inference and fast adaptation,” said Dr. Yuval Hart. “This computational trade-off proved to be a fruitful framework for explaining many of the neural and behavioural characteristics seen in autism.”
The researchers found that an increased dynamic range, indicating a gradual response of a neuronal population to changes in input, accounts for neural and behavioural variations in individuals diagnosed with autism across diverse tasks. This gradual response enables more accurate encoding of details but comes with a trade-off: slower adaptation to changes. By contrast, a narrower dynamic range allows for quick, threshold-based reactions, facilitating fast adaptation but potentially at the expense of fine discrimination.
Testing their model across diverse simulations and behavioural tasks, including finger-tapping synchronization, orientation reproduction, and global motion coherence, the researchers demonstrated that increased dynamic range might underlie specific autism r-related behaviours. This variation in response could stem from differences in how individual neurons activate. For instance, increased variability in individual neurons’ half-activation point, where the neuron’s response is half of its maximal value, could lead to a broader dynamic range at the population level, influencing how sensory input is processed and interpreted by the brain.
“We show how heterogeneity in the half-activation points of single neurons can result in a more gradual population response and can thus lead to an increased dynamic range,” explained Oded Wertheimer. “Given the vast literature that maps autism to mutations in genes related to neuronal receptors, the proposed biological mechanism is highly relevant – many sources of heterogeneity in these neuronal features can lead to increased dynamic range. This model provides a new lens for understanding autism spectrum disorder that bridges biological mechanisms at the neuronal level with computational principles.”
Dr. Hart and Wertheimer’s findings also provide insight into why autism spectrum disorder research often yields conflicting results. Differences in the dynamic range within the autism spectrum disorder population may contribute to the variation in findings across studies, highlighting the need for larger participant groups to ensure robust results.
Their model aligns with existing theories that relate autism spectrum disorder to atypical sensory processing, supporting a connection to broader biological and genetic factors. Specific genetic mutations associated with autism spectrum disorder, such as those affecting synaptic regulation, may contribute to this increased dynamic range. These biological factors could lead to a more variable neuronal response, creating the nuanced, analogue-like encoding seen in individuals with autism spectrum disorder individuals.
By exploring this computational trade-off, the study not only introduces a new perspective on autism spectrum disorder but also suggests future directions for study. The researchers propose that examining this dynamic range at different developmental stages or through animal models could further clarify its impact on autism spectrum disorder-related behaviors.
“The Samantha Craft Unofficial Checklist for Autism or Asperger’s in Females (I’ve seen this re-named a lot online!) or Autistic Checklist is one of the first checklists I reviewed with you on my channel. Something that has been of interest to me lately is how much these unofficial lists can hold up to the criteria recognized by diagnostic manuals. So, I thought it might be interesting to start here with this checklist and compare it to criteria in the DSM-5. If you all are interested, I may also compare it to the ICD-11.”
Children’s books often feature animal characters whose antics capture the hearts and inspire the imaginations of their young readers.
However, a new study has shown that iconic characters such as Peter Rabbit – or Toad and Ratty from The Wind in the Willows – can also play an essential role in children’s psychological development.
The research explored the extent to which different non-human characters influence children’s theory of mind skills, which include the ability to read and predict social changes in the environment through tone of voice, choice of words, or facial expression.
For the study, more than 100 children aged between five and ten were tested on their theory of mind skills when presented with stories featuring animal characters rather than human ones.
The study found that when faced with human characters, there was a clear age-related progression, with older children consistently outperforming their younger counterparts. Year 3 children performed better than the researchers had predicted in the tests featuring human characters.
However, in tests that involved animal characters, Year 1 participants were able to match the scores achieved by pupils from Year 3, who were two years older than them.
Dr Gray Atherton and Dr Liam Cross from the University of Plymouth’s School of Psychology led the research.
Dr Atherton, lead author of the new study, said: “Animals play a huge part in children’s stories, whether in books and comics or through TV and film. We wanted to test if that is down to more than simply liking the characters, whether there are actual benefits of children learning through watching or reading about animals, and if this changes over time. Our findings showed that human and non-human characters are important in helping children interpret the world around them and play differing roles at different developmental stages. Adapting activities and lessons in nurseries and the early school years to take that into account could be hugely effective in helping to support their development.”
The research builds on previous studies by Dr Atherton and Dr Cross, which explored factors that can influence the educational and social development of people with autism and learning difficulties.
These have included initiatives showing that playing board and online games can boost confidence among people with autism and others, highlighting that people with dyslexia and dyscalculia show reduced bias against others based on characteristics such as their disability, race or gender.
Based on the new research, the academics intend to explore in more detail whether their findings could specifically benefit children with such conditions.
Dr Cross added: “We believe this new study could be of particular importance for people with autism or other conditions that can impact their learning. Working with teenagers in the past, we have noticed how tasks that involve animal characters can result in autistic people performing just as well as non-autistic children. It would be interesting to replicate our current study with autistic children to understand if we can find more effective ways to support them at a critical point in their development.”
PhD student Inbar Fischer Credit Tel Aviv University
A groundbreaking study from Tel Aviv University enhances our understanding of the biological mechanisms behind genetically based autism. It mainly focuses on mutations in the SHANK3 gene, which are responsible for nearly one million autism cases worldwide. Based on these findings, the research team applied a genetic treatment that improved the functioning of cells affected by the mutation, paving the way for future therapies for SHANK3-related autism.
The study was led by the lab of Prof. Boaz Barak and PhD student Inbar Fischer from the Sagol School of Neuroscience and the School of Psychological Sciences at Tel Aviv University.
Prof. Barak: “Autism is a common neurodevelopmental disorder affecting 1-2% of the global population, with one in every 36 boys in the U.S. diagnosed. Its causes include environmental, genetic, and social factors, such as advancing parental age at conception. In my lab, we focus on the genetic causes of autism, particularly mutations in the SHANK3 gene. This gene is vital for the protein that binds receptors in neurons, essential for receiving chemical signals that enable neuron communication. Damage to SHANK3 can disrupt this communication, impairing brain development and function. Our study aims to explore previously unknown mechanisms through which SHANK3 mutations affect brain development, leading to autism.”
Specifically, the research team focused on two components in the brain that have not yet been studied extensively in this context: non-neuronal brain cells (glia) called oligodendrocytes and the myelin they produce. Myelin tissue is a fatty layer that insulates nerve fibres (axons), similar to the insulating layer that coats electrical cables. When the myelin is faulty, the electrical signals transmitted through the axons may leak, disrupting the message transmission between brain regions and impairing brain function.
The team employed a genetically engineered mouse model for autism, introducing a mutation in the Shank3 gene that mirrors the mutation found in humans with this form of autism. Inbar Fischer: “Through this model, we found that the mutation causes a dual impairment in the brain’s development and proper function: first, in oligodendrocytes, as in neurons, the SHANK3 protein is essential for the binding and functioning of receptors that receive chemical signals (neurotransmitters and others) from neighbouring cells. This means that the defective protein associated with autism disrupts message transmission to these vital support cells. Secondly, when the function and development of oligodendrocytes is impaired, their myelin production is also disrupted. The faulty myelin does not properly insulate the neuron’s axons, thereby reducing the efficiency of electrical signal transmission between brain cells and the synchronization of electrical activity between different brain parts. In our model, we found myelin impairment in multiple brain areas and observed that the animals’ behaviour was adversely affected.”
The researchers then sought a method for fixing the damage caused by the mutation, hoping to develop a treatment for humans ultimately. Inbar Fischer: “We obtained oligodendrocytes from the brain of a mouse with a Shank3 mutation and inserted DNA segments containing the normal human SHANK3 sequence. Our goal was to allow the normal gene to encode a functional and normal protein, which would perform its essential role in the cell by replacing the defective protein. To our delight, following treatment, the cells expressed the normal SHANK3 protein, enabling the construction of a functional protein substrate to bind the receptors that receive electrical signals. In other words, the genetic treatment we had developed repaired the oligodendrocytes’ communication sites, essential for the cells’ proper development and function as myelin producers.”
To validate findings from the mouse model, the research team generated induced pluripotent stem cells from the skin cells of a girl with autism caused by a SHANK3 gene mutation identical to that in the mice. From these stem cells, they derived human oligodendrocytes with the same genetic profile. These oligodendrocytes displayed impairments similar to those observed in their mouse counterparts.
Prof. Barak concludes: “In our study, we discovered two new brain mechanisms involved in genetically induced autism: damage to oligodendrocytes and, consequently, damage to the myelin they produce. These findings have important implications – both clinical and scientific. Scientifically, we learned that defective myelin played a significant role in autism and identified the mechanism causing the damage to myelin. Additionally, we revealed a new role for the SHANK3 protein: building and maintaining a functional binding substrate for receptors critical for message reception in oligodendrocytes (not just in neurons). We discovered that contrary to the prevailing view, these cells play essential roles in their own right, far beyond the support they provide for neurons — often seen as the leading players in the brain. In the clinical sphere, we validated a gene therapy approach that led to significantly improved development and function of oligodendrocytes derived from the brains of mice modelling autism. This finding offers hope for developing genetic treatment for humans, which could enhance the myelin production process in the brain. Furthermore, recognizing the significance of myelin impairment in autism—whether linked to the SHANK3 gene or not—opens new pathways for understanding the brain mechanisms underlying autism and paves the way for future treatment development.