Browse our Research Articles

Bidirectional modulation of the activity of the synaptic protein mGluR5 alters spontaneous mouse motor behavior and produces correlated changes in co-activity patterns among direct pathway neurons in the dorsal striatum.

Developmentally-based directed differentiation from cortical progenitors sets a foundation for in vitro mechanistic and therapeutic disease modeling, and toward regenerative neuronal repopulation and circuit repair.

Upregulation of the β subunit of translation initiation factor eIF2 underlies autophagy suppression and premature aging caused by disruption of axonal transport of mitochondria.

Deep behavioral phenotyping reveals that performance readouts from single-valence conditioning are biased by baseline sex differences in exploration, and mixed-valence conditioning provides a clearer assessment of learning in both sexes.

Combining statistical modeling with flow cytometry enables reliable, high-throughput quantification of division asymmetry in live cells, revealing how partitioning noise may shape tumor cell heterogeneity.

In individuals who started antiretroviral therapy during acute HIV infection, the proliferative capacity of HIV-specific CD8+ T-cells at 24 weeks of therapy predicted the subsequent reduction in the viral reservoir.

In a randomized trial, ART intensification by doubling the dolutegravir dosage in people with HIV stably suppressed on dolutegravir-based ART reduced levels of four HIV reservoir markers in peripheral blood.

A computational model of the striatal dopamine system predicts transporter expression and organisation as key determinants of regional striatal dopamine dynamics and distinct signal decoding by D1 and D2 receptors.

Single-cell transcriptomic analysis of the murine testicular interstitium across the lifespan reveals Cd34⁺/Sox4⁺ mesenchymal cells as Leydig progenitors, whose aging-associated decline in glutathione and Sox4-regulated regenerative capacity inform potential therapeutic strategies for age-related testicular dysfunction.

Genetic and electrophysiological studies uncover a mechanism linking a TTN missense variant to atrial fibrillation by coupling titin with potassium channel remodeling, revealing FHL2 as a modulator and therapeutic target.