Stanford researchers find the human brain actually grows from two separate organs

The human brain does not grow from one unified starting point, according to Stanford Medicine researchers who traced its earliest embryonic cells back to two separate progenitor systems that never overlap at any point in development. Kyle Loh, PhD, an associate professor of developmental biology who led the work, found that the front of the brain and the back of the brain arise from entirely different cell populations from the earliest embryonic stages onward.

The findings, published Sept. 18, 2026, in Nature Neuroscience, effectively describe two organs fused into what has always been treated as one, with co-first authors Rayyan Jokhai and Carolyn Dundes, both Stanford graduate students, running the experiments that traced each lineage. Collaborators at the California Institute of Technology and the University of California, San Francisco contributed to the work as well, broadening it beyond a single lab’s cell lines.

Two progenitor cell systems that never overlap

The Stanford Report’s account of the study describes cells expressing the gene Otx2 as the source of the forebrain and midbrain, the regions behind language, abstract thought and higher cognition. A separate population expressing the gene Gbx2 gives rise to the hindbrain instead, the region that runs automatic functions like breathing, heartbeat and swallowing. Loh summarized the split directly: “The front of the brain arises from a totally different progenitor cell than the back of the brain.”

The two cell populations carry fundamentally different chromatin configurations, the molecular packaging that determines which genes a cell can switch on. That difference locks each population into its developmental path from the start, according to the paper in Nature Neuroscience, co-authored with collaborators at Caltech and UCSF.

The decades-old lab failure this discovery explains

Labs have tried for decades to grow human hindbrain neurons and mostly failed. Co-first author Rayyan Jokhai said those earlier attempts likely tried to coax forebrain and midbrain progenitor cells into becoming hindbrain cells, a conversion the new study shows is not possible, according to Stanford Medicine’s release on the findings.

That single misassumption, treating the brain’s progenitor pool as one interchangeable stock rather than two lineages locked in from the start, is what kept hindbrain neurons out of reach in a dish for years despite repeated attempts across multiple labs and reprogramming techniques. Once the Stanford team started from the correct starting population instead of trying to force one lineage into becoming the other, the hindbrain cells it produced behaved like the real thing rather than an imperfect stand-in.

Growing hindbrain neurons in a dish for the first time

Starting from Gbx2-expressing progenitors instead of trying to convert forebrain cells, Loh’s team produced functional human hindbrain motor neurons in a petri dish for the first time. Loh described the practical result as a way to grow neurons from the back of the brain and study their functions directly, rather than relying only on animal models or postmortem tissue.

Stanford Medicine’s release also flags a further use for the same cell-source approach: because the hindbrain contains the circuits that regulate hunger, the newly isolated progenitor line could eventually support research into weight-control biology, a possibility the researchers describe as exploratory rather than an established application of the current findings. Getting from an isolated progenitor cell to a therapy or a validated research model typically takes years of additional work, and nothing in the current paper claims that timeline has shortened.

What it could mean for ALS and spinal muscular atrophy

Hindbrain motor neurons grown in a dish give researchers a direct way to study diseases that specifically degrade that region. The National Institute of Neurological Disorders and Stroke describes amyotrophic lateral sclerosis, or ALS, as a disorder that destroys the motor neurons controlling voluntary muscle movement, including breathing; roughly 90% of cases arise with no family history at all, and most people survive three to five years after symptoms begin.

Spinal muscular atrophy, the other disease Stanford’s release names as a target, is a leading genetic cause of death in infants, and both conditions compromise swallowing and breathing as hindbrain motor neurons fail. Researchers studying either disease have historically had to infer what is happening inside a human hindbrain motor neuron from animal models or from tissue examined only after death, neither of which shows the cell behaving in real time.

Whether lab-grown hindbrain neurons translate into an actual treatment for either disease remains untested. ScienceDaily’s coverage of the paper frames what the Nature Neuroscience study actually establishes as a new cell source to work from, not a therapy in itself, and the researchers funded by the National Institutes of Health and the Spinal Muscular Atrophy Foundation are positioning the discovery as the starting point for that longer-term work rather than its conclusion.

This article was produced with the assistance of AI and reviewed by Morning Overview editors prior to publication.

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