Before birth, an average of 25.9 percent of neurons in the human cerebral cortex carry large duplications or deletions of DNA, and in some brains the share reaches nearly half. After birth the average falls to 6.2 percent. A team from Harvard Medical School and Boston Children’s Hospital reports that the drop comes from the selective removal of the flawed cells.
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The finding, published in Nature on October 28, 2026, casts the perinatal period as a quality-control checkpoint for the genome. Diane Shao, a co-first author, summarized the result in one sentence: the brain is selecting for genomic integrity. Her co-authors Peter Park and Christopher Walsh led the work as senior authors.
Counting broken genomes one neuron at a time
The damage in question is called a copy number variant, a stretch of DNA that is duplicated or deleted. These variants are linked to autism, schizophrenia, epilepsy and intellectual disability, which is why finding so many in healthy fetal tissue surprised the group. According to the News-Medical report of the Harvard release, the team built a cheaper way to sequence single neurons lightly rather than deeply, then used it on 1,526 neurons from 16 individuals.
To check the light-touch method, the researchers sequenced 831 neurons from 12 individuals more deeply, and they profiled DNA and RNA from 44,861 individual cells to see which gene pathways differ in the cells that carried the variants. Park, a professor of biomedical informatics at Harvard’s Blavatnik Institute, put the prenatal range in his own words: between 13 and 46 percent of neurons in the developing brain are riddled with copy number variants. Walsh, a Bullard Professor of Pediatrics and Neurology at Boston Children’s Hospital and a Howard Hughes Medical Institute investigator, said the team was totally unprepared for how common the variants were in early development.
An earlier bioRxiv version of the work gives the shape of the sample more fully: donors from gestational week 14 to age 90, with the prenatal average of 25.9 percent spanning 12.7 to 46.0 percent across individual brains. That version counted 1,327 neurons in its main sequencing set, a figure the published release updates to 1,526. It also reported that the share of neurons with any copy number variant fell from about 63 percent before birth to about 29 percent after.
From 25.9 percent to 6.2 percent
The central contrast is between the prenatal average of 25.9 percent and the postnatal average of 6.2 percent, a drop of roughly four-fold. Both numbers are averages across donors, and the prenatal range shows how much one brain can differ from another. The preprint also found that the decline continues slowly through adult life, which fits the release’s statement that flawed neurons keep being removed into adulthood, only at a lower rate.
The authors do not claim to have watched cells die. The elimination is inferred from the before-and-after comparison across different people, since a living human cortex cannot be sampled twice. The release describes the removal of “the vast majority” of the flawed neurons as qualitative, not a measured elimination rate.
Losing the fight for synapses
Why would those neurons be the ones to go? Neurons with widespread variants showed abnormal expression of genes involved in building and maintaining synapses, and the authors suggest such cells lose out in the competition for connections, a known process in which neurons that fail to wire up usually die. The Neuroscience News summary likewise reports disrupted expression of the genes needed to build and maintain synapses, and the preprint adds more activity in cell-death pathways in high-burden cells. The group calls the synapse-competition explanation likely rather than proven, and it rests on gene-expression data.
The preprint says the variants arise in dividing progenitor cells, tying the breakpoints to early-replicating regions of the genome, which is consistent with stress during DNA copying. The preprint further found that stretches of the genome that stay free of deletions are rich in autism-related and postsynaptic genes, which suggests selection is strongest where the genes matter most for wiring.
Some variation survives in healthy adult brains. Whether that residue is an accident that slipped past the filter or does something useful is unknown, and the release lists it as an open question.
Mechanism, not diagnosis: Shao’s open questions
Shao, who is an instructor of neurology at Boston Children’s Hospital, said that understanding the mechanism could eventually point to what to look for and perhaps what to protect. She is listed in the Boston Children’s directory. The team is now asking whether elimination differs in people with autism and other neurodevelopmental conditions, where synaptic pruning is already known to be dysregulated, and whether the process contributes to neuron loss in diseases such as Alzheimer’s. Both ideas are hypotheses.
The samples are modest in size and come from tissue banks, hundreds to thousands of neurons from a limited number of donors, and the figures are for the cortex only. The paper itself, Perinatal elimination of genetically aberrant human cortical neurons, carries the full methods. Until a larger set of donors confirms the 25.9 and 6.2 percent averages, they describe the people sampled, not every brain.
This article was produced with the assistance of AI and reviewed by Morning Overview editors prior to publication.
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