A 2025 Stanford study suggests that the same changes that built the human brain may also explain why autism is so much more common in us than in other apes. The real story, though, is more interesting than the headlines.
Here is a puzzle worth sitting with for a moment. Autism is common in humans and almost never seen in other great apes. About one in 31 children in the United States has been identified as autistic, and the World Health Organization puts the global figure at roughly one in 100. In other primates, the behaviours we associate with autism barely show up at all — and they tend to involve abilities, like producing and understanding speech, that are unique to humans or far stronger in us. So why does autism seem to be such a human thing?
Two Stanford researchers, Alexander Starr and Hunter Fraser, have offered one of the more thought-provoking answers in years. Writing in Molecular Biology and Evolution, they don’t treat autism as a glitch in the system. They suggest something stranger: that it may be tied to the very changes that made human thinking what it is.
A rule about neurons — and the one that breaks it
Their starting point is simple enough. The most common neuron types in the brain ought to be the ones evolution leaves alone. They do important work, lots of cells depend on them, and tinkering is risky — so you’d expect them to barely change over millions of years. When Starr and Fraser checked this against data from three regions of the mammalian neocortex, the pattern held up: the more abundant a neuron type, the more stable it tends to be across species.
And then they hit the exception. The single most common neuron type in the neocortex — the layer 2/3 intratelencephalic excitatory neuron — has evolved unusually fast in humans compared with other apes. It should have been one of the quiet, conserved ones. In our lineage, it did the opposite.
Where autism comes in
That burst of change went hand in hand with something else: a set of genes linked to autism became quieter, turned down rather than off. Starr and Fraser’s argument is that the high rate of autism in humans may follow directly from natural selection for lower activity in this group of genes — genes that gave our ancestors some advantage, while also leaving a very common type of neuron more sensitive to disturbance.
This is the trade-off at the centre of their paper. The same genetic dialling-down that may have sharpened human cognition could also have made the system more delicate — so that a relatively small genetic or developmental nudge produces a bigger effect in us than it would in another animal.
What we might have gained from the bargain
If there was a price, there was presumably also something bought. And the candidates are not small. The changes the authors describe may have slowed brain development in childhood while supporting language and cognition — the kind of shift that could have fed both the variety of human minds and the rise of complex thought. A longer, slower childhood gives us more time to learn. And richer language is, tellingly, one of the areas most often affected in autism. Read this way, autism looks less like an error and more like one possible outcome of the same process that gave our species its distinctive abilities.
An open question, not a tidy answer
Here is where it pays to read carefully, because the most interesting thing in the paper is a question the authors deliberately leave open — not a conclusion they hand you. Starr lays out two possibilities. Did turning down those autism-linked genes push humans closer to an autism-like profile? Or did it instead make our gene-regulatory and neural networks more sensitive, so that genetic or environmental changes simply have larger effects on human cognition than the same change would elsewhere? Those are genuinely different claims, and the evidence so far doesn’t settle which one is right.
The study has its limits, too, and the authors are upfront about them. The ape comparison rested on small numbers of animals, and the lab-grown neural tissue used to compare humans and chimps reflects an early stage of development rather than a finished brain. It’s also worth keeping in mind that much of the rise in autism diagnoses over recent decades has been linked to better diagnosis and wider public awareness — a useful reminder that “prevalence” is never pure biology. It’s also about who gets noticed, and counted.
Biology is one layer, not the whole
A study like this is about where autism comes from, not about what it is like to live with — and it’s worth not blurring the two. The most elegant evolutionary account in the world tells you nothing about what an autistic child needs from their classroom, or what an autistic adult needs from a job or a relationship. The biology is real and worth understanding on its own terms. So is the fact that an autistic life is shaped by whether the world around it makes room, by the daily cost of bending to non-autistic expectations, and by all the ordinary things that make up any particular person.
What this research adds is a sharper view of one piece of the picture: how a common neuron type and a cluster of related genes may have shifted under selection in our lineage, and why that might matter for how often autism shows up in humans. Set beside the social and personal sides of the story, rather than standing in for them, it makes the underlying biology a little less mysterious — without pretending to explain the whole of what it means to be autistic.
Alexander L Starr, Hunter B Fraser, A General Principle of Neuronal Evolution Reveals a Human-Accelerated Neuron Type Potentially Underlying the High Prevalence of Autism in Humans, Molecular Biology and Evolution, Volume 42, Issue 9, September 2025, msaf189, https://doi.org/10.1093/molbev/msaf189
The European Autist 