SummaryAxon injury leads to rapid depletion of NAD-biosynthetic enzyme NMNAT2 and high levels of its substrate, NMN. We proposed a key role for NMN in Wallerian degeneration but downstream events and their relationship to other mediators remain unclear. Here, we show, in vitro and in vivo, that axotomy leads to a late increase in intra-axonal Ca2+, abolished by pharmacological or genetic reduction of NMN levels. NMN requires the pro-degenerative protein SARM1 to stimulate Ca2+ influx and axon degeneration. While inhibition of NMN synthesis and SARM1 deletion block Ca2+ rise and preserve axonal integrity, they fail to prevent early mitochondrial dynamic changes. Furthermore, depolarizing mitochondria does not alter the rate of Wallerian dege...
Traditionally, researchers have believed that axons are highly dependent on their cell bodies for lo...
The molecular triggers for axon degeneration remain unknown. We identify endogenous Nmnat2 as a labi...
Wld(S) (slow Wallerian degeneration) is a remarkable protein that can suppress Wallerian degeneratio...
Axon injury leads to rapid depletion of NAD-biosynthetic enzyme NMNAT2 and high levels of its substr...
SummaryAxon injury leads to rapid depletion of NAD-biosynthetic enzyme NMNAT2 and high levels of its...
Wallerian degeneration of physically injured axons involves a well-defined molecular pathway linking...
Wallerian degeneration of physically injured axons involves a well-defined molecular pathway linking...
Axons require the axonal NAD-synthesizing enzyme NMNAT2 to survive. Injury or genetically-induced de...
Axons require the axonal NAD-synthesizing enzyme NMNAT2 to survive. Injury or genetically induced de...
SARM1 function and nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2) loss both promote axon...
Wallerian degeneration (WD) is a conserved axonal self-destruction program implicated in several neu...
SummarySARM1 function and nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2) loss both promo...
Axon loss is a characteristic feature shared among various neurodegenerative disorders, regardless o...
Traditionally, researchers have believed that axons are highly dependent on their cell bodies for lo...
The molecular triggers for axon degeneration remain unknown. We identify endogenous Nmnat2 as a labi...
Wld(S) (slow Wallerian degeneration) is a remarkable protein that can suppress Wallerian degeneratio...
Axon injury leads to rapid depletion of NAD-biosynthetic enzyme NMNAT2 and high levels of its substr...
SummaryAxon injury leads to rapid depletion of NAD-biosynthetic enzyme NMNAT2 and high levels of its...
Wallerian degeneration of physically injured axons involves a well-defined molecular pathway linking...
Wallerian degeneration of physically injured axons involves a well-defined molecular pathway linking...
Axons require the axonal NAD-synthesizing enzyme NMNAT2 to survive. Injury or genetically-induced de...
Axons require the axonal NAD-synthesizing enzyme NMNAT2 to survive. Injury or genetically induced de...
SARM1 function and nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2) loss both promote axon...
Wallerian degeneration (WD) is a conserved axonal self-destruction program implicated in several neu...
SummarySARM1 function and nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2) loss both promo...
Axon loss is a characteristic feature shared among various neurodegenerative disorders, regardless o...
Traditionally, researchers have believed that axons are highly dependent on their cell bodies for lo...
The molecular triggers for axon degeneration remain unknown. We identify endogenous Nmnat2 as a labi...
Wld(S) (slow Wallerian degeneration) is a remarkable protein that can suppress Wallerian degeneratio...