Giuseppe Orsomando

This study shows that SARM1 activation causes mitochondrial dysfunction in human neurons, which can be reversed by nicotinamide or prevented by antisense oligonucleotides.

This study shows that low NMNAT2 levels cause sub-lethal SARM1 activation and reduce the effectiveness of nicotinamide riboside in axons, leading to axonal defects and behavioral changes in mice.

The paper adapts a commercial NAD quantification kit to measure SARM1 base exchange activity using an NAD analog, offering a rapid and sensitive method.

This study shows that reducing NMN levels in Drosophila prevents axon degeneration and neurodegeneration, revealing NMN's role in axon injury and disease.

This study identifies VMN, a metabolite of the pesticide vacor, as a potent SARM1 activator, showing that SARM1 removal rescues vacor-induced neuron and axon death.

This study shows mitochondrial impairment triggers Wallerian-like axon degeneration by depleting NMNAT2, activating SARM1, and replicating key steps of the Wallerian pathway in mice and flies.

The paper identifies biallelic NMNAT2 mutations in two fetuses with FADS, showing their role in axon survival and linking them to Wallerian degeneration.

The paper identifies a homozygous NMNAT2 mutation causing polyneuropathy and erythromelalgia in two sisters, linking it to axon degeneration and supporting the role of the Wallerian pathway in human disease.