Yo Sasaki

This study shows that deleting Sarm1 reduces axonal degeneration in a CMT2J mouse model, but does not fully prevent disease progression.

This study shows that enhancing mitochondrial NAD+ import through SLC25A51 protects neurons from SARM1-driven degeneration by preventing coupled metabolic failure.

The paper investigates how partial disruption of lactate metabolism, specifically through LDHB loss, synergizes with ALS genetic risk factors to accelerate motor decline.

This study shows SARM1 is essential for neuronal Parthanatos, a cell death pathway triggered by DNA damage and linked to neurodegenerative diseases.

The paper shows that overexpressing ABHD12 in neurons reduces macrophage activation and preserves axon integrity in a sarmopathy model by modulating phosphatidylserine levels.

This study quantifies SARM1 activity in human PBMCs using agonists and inhibitors, showing dose-dependent cAPDR increases and potential for clinical readouts.

This study shows that macrophage depletion reverses neuropathic symptoms in a mouse model of SARM1-dependent neuropathy caused by NMNAT2 variants.

This study shows that disrupting lactate metabolism in Schwann cells or motor neurons causes motor axon degeneration, while sensory axons remain unaffected, highlighting a specific dependency of motor axons on lactate shuttling.

This study shows that SARM1 inhibition reduces axonal, synaptic, and mitochondrial defects in a CMT2A rat model.

The paper develops a P0T124M mouse model of CMT2J neuropathy, showing axonal damage without significant myelin defects and altered axo-glia communication.

The paper identifies constitutively active SARM1 variants in ALS patients that induce neuropathy and neuroinflammation in mice.

This study uses live imaging to show that SARM1 activation leads to a sequence of cellular events starting with ATP loss and ending in axonal self-destruction.

This study identifies neurotoxins that activate SARM1 by binding to its allosteric site, leading to NAD+ depletion and neuronal death.

The paper identifies nicotinic acid mononucleotide (NaMN) as an allosteric inhibitor of SARM1 that promotes axonal protection by blocking NMN binding and stabilizing the inactive SARM1 conformation.

This study shows that SARM1 depletion prevents NMNAT1-dependent photoreceptor death and retinal degeneration in mice, identifying SARM1 as a therapeutic target for retinopathies.