The human brain does not form from a single type of cell, but from two populations of neural progenitors that arise along parallel pathways from the earliest stages of the embryo, according to a Stanford University study published on September 18, 2026 in Nature Neuroscience.
The finding contradicts the model that dominated developmental biology for decades: the idea that a single progenitor cell of the neural ectoderm gives rise to the entire brain, an assumption that attributed a common evolutionary origin to all of its regions. The Stanford team identified two populations that do not overlap at any point: one marked by the Otx2 gene, destined for the forebrain and midbrain, where language and abstract reasoning reside, and another marked by Gbx2, which forms the hindbrain, the region that governs breathing, heart rate and sleep. In Mexico, the finding coincides with accelerated aging: 10% of the population is already 65 or older, according to the 2025 Intercensal Survey by INEGI released on September 22.
The experiments, conducted in mouse embryos during gastrulation, showed that both populations present distinct chromatin configurations within the first 48 hours of differentiation, a trait that fixes the fate of each lineage. That separation explains why for decades it was so difficult to culture human hindbrain neurons in the laboratory: previous attempts sought to convert forebrain progenitors into posterior cells, a path that the study shows to be unviable. By reproducing the posterior route, the team generated functional motor neurons from rhombomeres 5 and 6 of the human hindbrain, capable of producing action potentials. The Otx/Gbx pattern also appears in chickens, zebrafish and acorn worms, which points to an antiquity of more than 500 million years. Among the diseases that this model makes it possible to investigate are spinal muscular atrophy and amyotrophic lateral sclerosis, notes Investigación y Desarrollo.
With that model, the laboratory of Kyle Loh, associate professor of developmental biology, now seeks to understand how the motor neurons of the brainstem degrade, a step prior to any regenerative therapy for spinal muscular atrophy and amyotrophic lateral sclerosis. The next target is the hindbrain's hunger circuits, the same ones that regulate appetite.
This article was written with the assistance of artificial intelligence based on verified sources and reviewed by a human editor before publication.
