Yurie Yamada

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 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 loss of STMN2, linked to TDP-43 pathology in ALS, causes motor neuropathy with NMJ denervation in mice.

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

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