Hui‐Chen Lu

This paper develops a human myelin microphysiological system to test treatment responses in multiple sclerosis patients, showing differential demyelination and immune responses between patient groups.

This study shows that NMNAT2 loss disrupts APP processing in neurons by causing redox failure and proteostasis disruption, with SARM1 playing a key role in this process.

This study shows that perinatal CBD exposure alters astrocyte morphology and tripartite synapse organization in a sex-dependent manner in the medial prefrontal cortex.

The paper identifies NMNAT2 regulatory elements and associated genes using 4C-seq and bioinformatics in human cells, showing correlations with mRNA levels in single-nuclei RNA-seq datasets.

The paper shows that loss of NMNAT2 in glutamatergic neurons causes metabolic shifts and neurodegeneration, which are mitigated by SARM1 deletion.

This study shows that GABAergic inputs refine neuronal subnetworks in the mouse primary somatosensory cortex, increasing their coherence as they mature.

This study investigates how prenatal methadone exposure affects protein and phosphoprotein levels in specific brain regions of mice, showing unique changes in the primary motor cortex linked to synaptic function.

This study shows NMNAT2 maintains NAD redox potential in axons to support glycolysis and fast transport, preventing axonal degeneration in mice.

This study shows that NMNAT2 deletion in cortical glutamatergic neurons causes neurodegeneration and disrupts cortical development, with Sarm1 loss partially rescuing these effects.

This study examines the effects of prenatal methadone exposure on mouse offspring, finding impairments in physical growth, sensorimotor behavior, and motor neuron function.