Amy M. Strickland

Mitochondrial NAD+ import gates neuronal resilience to active SARM1

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

Dysregulated lactate metabolism synergizes with ALS genetic risk factors to accelerate motor decline

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

Suppressing phagocyte activation by overexpressing the phosphatidylserine lipase ABHD12 preserves sarmopathic nerves

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

Reduced STMN2 and pathogenic TDP-43, two hallmarks of ALS, synergize to accelerate motor decline in mice

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

Macrophage depletion blocks congenital SARM1-dependent neuropathy

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

Disruption of lactate metabolism in the peripheral nervous system leads to motor-selective deficits

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.

Loss of Stathmin-2, a hallmark of TDP-43-associated ALS, causes motor neuropathy

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

SARM1 promotes axonal, synaptic, and mitochondrial pathologies in Charcot-Marie-Tooth disease type 2A

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

Constitutively active SARM1 variants found in ALS patients induce neuropathy

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

Neurotoxins subvert the allosteric activation mechanism of SARM1 to induce neuronal loss

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