Lee J. Martin

Injury-induced spinal motor neuron apoptosis is preceded by DNA single-strand breaks and is p53- and Bax-dependent.

Axonal transection in adult rat brain induces transsynaptic apoptosis and persistent atrophy of target neurons.

Long-term culture of mouse cortical neurons as a model for neuronal development, aging, and death.

Altered expression and phosphorylation of N-methyl-D-aspartate receptors in piglet striatum after hypoxia-ischemia.

Immature and mature cortical neurons engage different apoptotic mechanisms involving caspase-3 and the mitogen-activated protein kinase pathway.

Rapid subcellular redistribution of Bax precedes caspase-3 and endonuclease activation during excitotoxic neuronal apoptosis in rat brain.

DNA base-excision repair enzyme apurinic/apyrimidinic endonuclease/redox factor-1 is increased and competent in the brain and spinal cord of individuals with amyotrophic lateral sclerosis.

DNA damage profiling in motor neurons: a single-cell analysis by comet assay.

Early events of target deprivation/axotomy-induced neuronal apoptosis in vivo: oxidative stress, DNA damage, p53 phosphorylation and subcellular redistribution of death proteins.

Olfactory bulb core is a rich source of neural progenitor and stem cells in adult rodent and human.

Hypothermia for 24 hours after asphyxic cardiac arrest in piglets provides striatal neuroprotection that is sustained 10 days after rewarming.

Nitration of the striatal Na,K-ATPase alpha3 isoform occurs in normal brain development but is not increased during hypoxia-ischemia in newborn piglets.

Histopathological and behavioral characterization of a novel model of cardiac arrest and cardiopulmonary resuscitation in mice.

Neonatal mice lacking functional Fas death receptors are resistant to hypoxic-ischemic brain injury.

Pluripotent fates and tissue regenerative potential of adult olfactory bulb neural stem and progenitor cells.

In situ immunoradiographic method for quantification of specific proteins in normal and ischemic brain regions.

Adult motor neuron apoptosis is mediated by nitric oxide and Fas death receptor linked by DNA damage and p53 activation.

Apoptosis in perinatal hypoxic-ischemic brain injury: how important is it and should it be inhibited?

Transplanted human embryonic germ cell-derived neural stem cells replace neurons and oligodendrocytes in the forebrain of neonatal mice with excitotoxic brain damage.

Parkinson's disease alpha-synuclein transgenic mice develop neuronal mitochondrial degeneration and cell death.

The adult neural stem and progenitor cell niche is altered in amyotrophic lateral sclerosis mouse brain.

Amyotrophic lateral sclerosis 2-deficiency leads to neuronal degeneration in amyotrophic lateral sclerosis through altered AMPA receptor trafficking.

Motor neuron degeneration in amyotrophic lateral sclerosis mutant superoxide dismutase-1 transgenic mice: mechanisms of mitochondriopathy and cell death.

Mitochondriopathy in Parkinson disease and amyotrophic lateral sclerosis.

Dopamine receptor modulation of hypoxic-ischemic neuronal injury in striatum of newborn piglets.

Transgenic mice with human mutant genes causing Parkinson's disease and amyotrophic lateral sclerosis provide common insight into mechanisms of motor neuron selective vulnerability to degeneration.

Resistance to Alzheimer's pathology is associated with nuclear hypertrophy in neurons.

Rapid NMDA receptor phosphorylation and oxidative stress precede striatal neurodegeneration after hypoxic ischemia in newborn piglets and are attenuated with hypothermia.

Adult olfactory bulb neural precursor cell grafts provide temporary protection from motor neuron degeneration, improve motor function, and extend survival in amyotrophic lateral sclerosis mice.

Motor neuron disease occurring in a mutant dynactin mouse model is characterized by defects in vesicular trafficking.

DNA damage and repair: relevance to mechanisms of neurodegeneration.

Molecular regulation of DNA damage-induced apoptosis in neurons of cerebral cortex.

Delayed neural network degeneration after neonatal hypoxia-ischemia.

Glycinergic innervation of motoneurons is deficient in amyotrophic lateral sclerosis mice: a quantitative confocal analysis.

The mitochondrial permeability transition pore in motor neurons: involvement in the pathobiology of ALS mice.

The mitochondrial permeability transition pore: a molecular target for amyotrophic lateral sclerosis therapy.

Neuropathologic studies of the Baltimore Longitudinal Study of Aging (BLSA).

Sigma receptor ligand 4-phenyl-1-(4-phenylbutyl)-piperidine modulates neuronal nitric oxide synthase/postsynaptic density-95 coupling mechanisms and protects against neonatal ischemic degeneration of striatal neurons.

Inducible nitric oxide synthase is present in motor neuron mitochondria and Schwann cells and contributes to disease mechanisms in ALS mice.

Synphilin-1 attenuates neuronal degeneration in the A53T alpha-synuclein transgenic mouse model.

Skeletal muscle-restricted expression of human SOD1 causes motor neuron degeneration in transgenic mice.

Mitochondrial pathobiology in Parkinson's disease and amyotrophic lateral sclerosis.

Necrostatin decreases oxidative damage, inflammation, and injury after neonatal HI.

Olesoxime, a cholesterol-like neuroprotectant for the potential treatment of amyotrophic lateral sclerosis.

The mitochondrial permeability transition pore regulates nitric oxide-mediated apoptosis of neurons induced by target deprivation.

Mitochondrial and Cell Death Mechanisms in Neurodegenerative Diseases.

An approach to experimental synaptic pathology using green fluorescent protein-transgenic mice and gene knockout mice to show mitochondrial permeability transition pore-driven excitotoxicity in interneurons and motoneurons.

Glycine receptor channels in spinal motoneurons are abnormal in a transgenic mouse model of amyotrophic lateral sclerosis.

Neuronal cell death in neonatal hypoxia-ischemia.

Neuroprotective effect of acid-sensing ion channel inhibitor psalmotoxin-1 after hypoxia-ischemia in newborn piglet striatum.

Motoneuron subtypes show specificity in glycine receptor channel abnormalities in a transgenic mouse model of amyotrophic lateral sclerosis.

Striatal neuroprotection from neonatal hypoxia-ischemia in piglets by antioxidant treatment with EUK-134 or edaravone.

Generation and characterization of transgenic mice expressing mitochondrial targeted red fluorescent protein selectively in neurons: modeling mitochondriopathy in excitotoxicity and amyotrophic lateral sclerosis.

Inhibitory synaptic regulation of motoneurons: a new target of disease mechanisms in amyotrophic lateral sclerosis.

Mitochondrial pathobiology in ALS.

Epigenetic regulation of motor neuron cell death through DNA methylation.

Nuclear localization of human SOD1 and mutant SOD1-specific disruption of survival motor neuron protein complex in transgenic amyotrophic lateral sclerosis mice.

Attenuation of neonatal ischemic brain damage using a 20-HETE synthesis inhibitor.

Biology of mitochondria in neurodegenerative diseases.

Programmed Necrosis: A Prominent Mechanism of Cell Death following Neonatal Brain Injury.

Early antioxidant treatment and delayed hypothermia after hypoxia-ischemia have no additive neuroprotection in newborn pigs.

Adenosine A2A receptor contributes to ischemic brain damage in newborn piglet.

Aberrant regulation of DNA methylation in amyotrophic lateral sclerosis: a new target of disease mechanisms.

Imaging neurodegeneration in the mouse hippocampus after neonatal hypoxia-ischemia using oscillating gradient diffusion MRI.

The olfactory bulb in newborn piglet is a reservoir of neural stem and progenitor cells.

Mitochondrial permeability transition pore regulates Parkinson's disease development in mutant α-synuclein transgenic mice.

Mitochondrial DNMT3A and DNA methylation in skeletal muscle and CNS of transgenic mouse models of ALS.

Skeletal muscle DNA damage precedes spinal motor neuron DNA damage in a mouse model of Spinal Muscular Atrophy (SMA).

Induced Pluripotent Stem Cells from Familial Alzheimer's Disease Patients Differentiate into Mature Neurons with Amyloidogenic Properties.

Oscillating gradient diffusion MRI reveals unique microstructural information in normal and hypoxia-ischemia injured mouse brains.

The non-human primate striatum undergoes marked prolonged remodeling during postnatal development.