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Neandertals were once portrayed as dull evolutionary failures, separated from modern humans by a wide intellectual gulf. Archaeology has steadily erased that caricature. They made sophisticated tools, processed plants into food, treated illness, used symbols and cared for their dead. Then the first Neandertal genome delivered an even more intimate correction in 2010: Neandertals and Homo sapiens interbred, and their DNA still forms part of many living human genomes.

Neuroscientist Emily L. Casanova and geneticist F. Alex Feltus explore the possibility that this inheritance reaches into the modern mind. Surviving Neandertal variants have been associated with brain anatomy, neural connectivity, mood, attention and autism. Yet the authors repeatedly stress that clinical paleogenomics is young. The emerging picture is not one in which a few ancient genes dictate personality or diagnosis. It is a complex story about small genetic effects interacting with one another, modern genomes and the environments in which brains develop.

Ancient Variants in a Modern Brain

Neandertal DNA has already been linked to immune function, blood clotting, metabolism, skin and hair traits, and vulnerability to several diseases. Its influence on the brain is less intuitive. Genes involved in neural development are often highly sensitive to harmful changes, so natural selection has removed much Neandertal ancestry from those regions of the human genome. Even so, some ancient variants have persisted in or near brain-related genes.

Their effects appear at several scales. People with more Neandertal ancestry are somewhat more likely to have an elongated skull shape reminiscent of Neandertals, particularly around the parietal and occipital regions. Some of the associated variants sit near genes involved in producing neurons and forming myelin, the insulation that helps nerve cells transmit signals over long distances.

Brain-imaging studies have also reported a possible trade-off. Greater Neandertal ancestry has been associated with stronger connectivity in pathways used for visual processing and weaker connectivity in neighboring pathways involved in social cognition. Another line of research focuses on the cerebellum. Once treated mainly as a center for movement and coordination, this structure is now known to contribute to attention, emotion, sensory processing and the ability to infer other people’s mental states. Reconstructions suggest that Neandertals had smaller cerebellums than early modern humans, raising the possibility that inherited variants still contribute modestly to variation in these functions today.

The population history behind those variants matters. Neandertals endured a severe, prolonged genetic bottleneck, with their population perhaps falling to roughly 5,000 individuals between 50,000 and 40,000 years ago. In a small, isolated population, mildly harmful mutations can spread by chance instead of being efficiently removed by natural selection. When the two human lineages interbred, Homo sapiens acquired some of that genetic legacy as well.

Researchers have since associated particular Neandertal variants with depression, sleep timing, substance use, pain sensitivity and attention-deficit hyperactivity disorder. These links are statistical rather than deterministic. A variant may slightly change susceptibility without being necessary or sufficient to produce a condition, and the same piece of DNA may have different consequences in different genetic and environmental settings.

The Autism Question

Casanova and Feltus are especially interested in autism. Their hypothesis grew from parallels between two bodies of evidence. In nonautistic people, greater Neandertal ancestry has been associated with enhanced visual pathways and reduced connectivity in some social-processing pathways. Autistic people can likewise show strong visuospatial skills alongside differences in social cognition, and both Neandertals and autistic people have been reported to have less volume in certain parts of the cerebellum.

The authors compared genetic data from autistic and nonautistic people while matching groups by ancestry, an essential precaution because Neandertal inheritance varies considerably among populations. They found that autistic participants did not carry more Neandertal DNA overall. Instead, they were more likely to carry certain rare Neandertal-derived single-nucleotide polymorphisms, or SNPs. The team also identified ancient variants that may alter gene activity in the brain, including candidates related to epilepsy and to the balance between excitatory and inhibitory neural signaling.

These findings do not establish that Neandertal DNA causes autism. The initial analysis covered only a small fraction of the genome, many candidate genes remain poorly understood, and an association can arise through mechanisms researchers have not yet identified. Autism itself is extraordinarily heterogeneous, and brain development emerges from regulatory networks involving tens of thousands of genes. The more plausible model is that interbreeding modified existing human systems rather than introducing a discrete Neandertal program for any modern diagnosis.

The authors plan to use complete family genomes to examine millions of regulatory sites, including regions between genes that control how strongly genes are expressed. They also intend to investigate Denisovan ancestry in populations that carry more DNA from those extinct relatives. Such work could reveal whether hybridization broadly reshaped human neurodevelopment and, eventually, identify pathways useful to personalized medicine.

Inheritance Is Not Destiny

Evolution does not sort every trait neatly into beneficial and harmful categories. Some rare Neandertal variants associated with autism or ADHD may be slowly disappearing because their carriers leave fewer descendants or simply because rare variants tend to vanish by chance in a large population. At the same time, related genetic patterns may persist because they accompany useful traits. Autism-associated variation has also been linked in some studies to visuospatial ability, memory, intelligence, creativity and educational achievement. Relatives of autistic people are disproportionately represented in scientific and technical careers and may help keep some of the same variants in the population.

That possibility should not be turned into another simplistic evolutionary tale. It neither romanticizes the challenges of neurodevelopmental conditions nor reduces people to ancient ancestry. Instead, it shows why the medical model of disability, focused exclusively on deficits to be corrected, can miss the trade-offs and diversity produced by evolution.

The article’s deepest point is that Neandertal DNA is not merely a relic tucked into the genome. It may still participate in the biological networks through which humans perceive, socialize, regulate emotion and develop distinctive cognitive profiles. The evidence remains preliminary, but it has already dissolved the boundary between “them” and “us.” Modern human minds arose not from an isolated lineage but from a history of migration, interbreeding and genetic exchange whose consequences are still unfolding.