Sen Yang

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.

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 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.