Researchers found that as certain brain cells evolved to enhance human cognition, their genetic activity also shifted in ways that may increase the likelihood of autistic traits.
The findings contribute to ongoing debate over the roots of autism, following controversial claims by the Trump administration linking the condition to paracetamol use during pregnancy, a claim widely disputed by experts.
Stanford University scientists Alexander Starr and Hunter Fraser, who led the research, said:
“Our results suggest that the origins of autism stretch far back, long before any recent man-made influences.”
The team examined different types of neurons in humans, chimpanzees, gorillas, rhesus macaques, marmosets and mice. Each cell contained DNA with tens of thousands of genes, but the activity levels of these genes varied, giving each neuron type a unique “fingerprint.”
By comparing these fingerprints across species, researchers estimated how much each neuron type had evolved over time. They observed a general pattern: the more common a neuron type in the brain, the more slowly it evolved. This stability is likely because harmful changes in abundant cells could have widespread effects.
However, one neuron type in humans broke this pattern. Layer 2/3 intratelencephalic excitatory neurons, or L2/3 IT neurons, are abundant in the outer layer of the human brain. They connect different brain regions and are thought to be key to human intelligence. The study suggests these neurons evolved unusually rapidly after humans diverged from chimpanzees around six to eight million years ago.
The researchers then analysed genes linked to increased autism risk, many of which guide how neurons connect and how the brain develops. In human L2/3 IT neurons, the activity of these genes had been dialled down. In other words, evolution boosted cognitive abilities while lowering the activity of genes that reduce the likelihood of autistic traits.
Starr explained:
“One guess is that these changes may have lengthened the time for human brain development, giving us more time to learn skills such as language and social interactions as these increase in complexity during human evolution.”
Published in the journal Molecular Biology and Evolution, the study presents this as an evolutionary trade-off. Small genetic or environmental factors are now sufficient to place individuals on the autistic spectrum. Such trade-offs are not uncommon in evolution: for example, the sickle cell mutation protects against malaria but causes serious illness when inherited in two copies.
In the case of L2/3 IT neurons, the trade-off may have been cognitive: sharper thinking and more sophisticated communication for humans as a species, alongside increased diversity in how individuals think and relate to others.
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