A. Joseph Bloom

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 identifies ATP8A2 as a TDP-43 target whose loss leads to PS exposure and neuroinflammation, suggesting immune cell inhibition as a therapeutic strategy for ALS-FTD and CAMRQ4.

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 shows that reduced STMN2 and pathogenic TDP-43 synergize to accelerate motor decline in mice without detectable neuropathology but with mitochondrial abnormalities.

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.

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

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