Michael P. Coleman

The paper identifies promoter variants in NMNAT2 and SARM1 that affect their transcription levels and may contribute to susceptibility to Programmed Axon Death.

This study identifies tau oligomers in the brains of individuals who died shortly after traumatic brain injury, suggesting an early pathological mechanism linked to Alzheimer's disease.

This study shows that SARM1 activation causes mitochondrial dysfunction in human neurons, which can be reversed by nicotinamide or prevented by antisense oligonucleotides.

This study shows that low NMNAT2 levels cause sub-lethal SARM1 activation and reduce the effectiveness of nicotinamide riboside in axons, leading to axonal defects and behavioral changes in mice.

This study shows that lowering glucose increases Aβ levels in mouse brain slices and human cells, likely via BACE1 activation, but not in hypoxia conditions.

The paper shows that genetically perturbed myelin increases neuroinflammation-driven axon degeneration through immune-glial interactions in mice.

This paper introduces a novel mouse myelinating Schwann cell-DRG coculture system to study axon protection and degradation after injury.

The paper shows SARM1 is present in oligodendrocytes but not Schwann cells, and its deletion does not affect myelination in zebrafish or mice.

This study shows that reducing NMN levels in Drosophila prevents axon degeneration and neurodegeneration, revealing NMN's role in axon injury and disease.

This study shows NMNAT2 maintains NAD redox potential in axons to support glycolysis and fast transport, preventing axonal degeneration in mice.

This study shows that NMNAT2 deletion in cortical glutamatergic neurons causes neurodegeneration and disrupts cortical development, with Sarm1 loss partially rescuing these effects.

This study identifies VMN, a metabolite of the pesticide vacor, as a potent SARM1 activator, showing that SARM1 removal rescues vacor-induced neuron and axon death.

This study uses MRI and histology to identify structural and cellular changes in TDP-43 knock-in mice, linking them to ALS-FTD pathology and identifying PV+ interneuron loss as a potential biomarker.

The paper investigates whether tau assemblies behave like independently acting prion-like particles in mouse neural tissue and finds that seeding behavior only occurs at supra-physiological concentrations.

This study shows that inhibiting GSK3 reduces TDP-43 levels and neurotoxicity in mammalian neurons by promoting TDP-43 turnover through a caspase-dependent mechanism.

This study shows HERV-K(HML-2) RNA activates TLR8 and Tlr7, causing neurodegeneration in mice and correlating with AD in humans.

This study shows that BACE1 inhibition reduces excessive vascular sprouting in AD by restoring NOTCH3 signaling and normalizing endothelial filopodia formation.

This study shows mitochondrial impairment triggers Wallerian-like axon degeneration by depleting NMNAT2, activating SARM1, and replicating key steps of the Wallerian pathway in mice and flies.

The paper identifies biallelic NMNAT2 mutations in two fetuses with FADS, showing their role in axon survival and linking them to Wallerian degeneration.

The paper identifies a homozygous NMNAT2 mutation causing polyneuropathy and erythromelalgia in two sisters, linking it to axon degeneration and supporting the role of the Wallerian pathway in human disease.

This study develops an organotypic hippocampal slice culture model of neuroinflammation and shows that LPS-induced synaptophysin loss depends on microglia and IL1β.