Sparse patterns in gene expression allow simultaneous discovery of cell states, lineage relationships and key genes controlling developmental decisions.

Impairing TDP-43 RNA-binding capacity through a single acetylation-mimic mutation alters TDP-43 function and recapitulates biochemical, molecular, and behavioral features of sporadic TDP-43 proteinopathies, thus providing opportunities for new research into pathogenic mechanisms and therapeutic interventions.

The structural maintenance of chromosomes complex, SMC5/6, is crucial for brain development and function as it ensures proficient DNA replication in neural progenitor cells prior to chromosome segregation.

Neurons mature slower in humans than in other non-human primates.

A human cellular model of a prototypical form of intractable childhood epilepsy supports selective impairment of inhibitory neurons as a key pathophysiological mechanism.

A vessel and brain fusion organoid model provides a platform for the study of interactions between neuronal and non-neuronal components during brain development and functioning.

Automated liquid handling, whole mount staining, and clearing allow unbiased 3D quantitation of cell markers in human neural organoids with diameters of up to 1 mm at the single-cell level.

Microcephaly-associated mutations disrupt microtubule-dependent WDR62 translocation from the Golgi complex to the mitotic spindle poles, impair mitotic progression, and alter neurogenic trajectories in patient induced Pluripotent Stem Cell-derived 2D and 3D models of human neurodevelopment.

Analyses based on the mouse model of a human genetic disease reveal that the neuron production of cerebral tissue can be boosted by escalated signaling between neural progenitors and the vasculature.

Neural progenitors in humans and chimpanzee organoids show remarkably similar cellular and molecular parameters, but metaphase is longer during human mitosis.