An epilepsy-associated potassium channel variant causes neuron-type-dependent alterations in ionic currents, neuronal excitability, and network connectivity.

Direct reprogramming of somatic cells to an inner ear sensory hair cell-like state provides an experimental platform to identify causes and treatments for hair cell loss and hearing deficits.

Polyglutamine expansion in mutant huntingtin disrupts a novel transcription-coupled DNA repair complex, providing an undescribed mechanism of neuronal toxicity and degeneration in Huntington's disease.

Loss of functional dystroglycan disrupts the formation and function of CCK⁺/CB₁R⁺ inhibitory synapses in hippocampal CA1, resulting in reduced seizure thresholds in mouse models of dystroglycanopathy.

While tau and aging have highly overlapping differential gene expression signatures, they diverge in the affected cell types, with aging having a wide-ranging impact and tau-triggered changes instead polarized to excitatory neurons and glia.

Diversification of human pacemaker subpopulations is directed by WNT and TGFβ signaling.

Behavioral and molecular mechanistic studies elaborate the important role of ErbB4 in noradrenergic neurons associated with mania pathogenesis.

mTOR signaling regulates the morphology of a human-enriched neural stem cell population and thus contributes to the radial architecture of the developing human cortex with implications for neurodevelopmental disease.

Non-coding mutations in microsatellite-instable (MSI) colorectal tumors are prevalent and activate cancer-specific enhancers, thereby disrupting gene expression control.