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School of Medicine
Lee J. Martin, Ph.D.
Curriculum Committee Chair, Graduate Program in Pathobiology
Professor of Pathology
Research Interests: Cell death signaling in neurological disease
Dr. Lee J. Martin is a professor of pathology in the division of neuropathology at the Johns Hopkins University School of Medicine. He has a secondary appointment in neuroscience. His research focuses on cell death signaling in neurological disease.
Dr. Martin is co-investigator in the Alzheimer’s Disease Research Center and is a member of the Graduate Program in Pathobiology at the Johns Hopkins School of Medicine.
His team is currently engaged in the use of animal and cell models of human neurodegenerative disease to unravel the mechanisms of neurodegeneration.
- Curriculum Committee Chair, Graduate Program in Pathobiology
- Co-Investigator, Neuropathology Core
- Professor of Pathology
- Professor of Neuroscience
Centers & Institutes
Research & Publications
Dr. Martin is studying mechanisms of neuronal death in adult and developing central nervous systems. He is testing the hypothesis that selective vulnerability (when only certain groups of neurons degenerate after an acute neurological insult) is dictated by brain regional connectivity, mitochondrial function and oxidative stress and is mediated by excitotoxic cell death resulting from abnormalities in excitatory, glutamatergic signal transduction pathways, including glutamate transporters and glutamate receptors as well as their downstream intracellular signaling molecules.
He is also investigating the contribution of neuronal/glial apoptosis and necrosis as cell death pathways in animal (including transgenic mice) models of acute and progressive neurodegeneration. Dr. Martin uses a variety of anatomical and molecular neurobiological approaches, including neuronal tract-tracing techniques, immunocytochemistry, immunoblotting, antipeptide antibody production, transmission electron microscopy, and DNA analysis to determine the precise regional and cellular vulnerabilities and the synaptic and molecular mechanisms that result in selective neuronal degeneration.
Martin LJ, Chang Q. "Inhibitory synaptic regulation of motoneurons: A new target of disease mechanisms in amyotrophic lateral sclerosis." Mol Neurobiol. 2012; 45: 30-42.
Chang Q, Martin LJ. "Motorneuron subtypes show specificity in glycine receptor channel abnormalities in a transgenic mouse model of amyotrophic lateral sclerosis." Channels. 2011 Jul-Aug;5(4):299-303. doi: 10.4161/chan.5.4.16206. Epub 2011 Jul 1.
O'Brien R, Resnick S, Zonderman A, Ferucci L, Crain B, Pletnikova O, Rudow G, Iacono D, Riudavets M, Driscoll I, Price D, Martin L, Troncoso J. "Neuropathologic studies of the Baltimore Longitudinal Study of Aging (BLSA)." J Alzheimers Dis. 2009;18(3):665-75. doi: 10.3233/JAD-2009-1179.
Laird F, Farah M, Ackerly S, Hoke A, Maragakis N, Rothstein J, Griffin J, Price DL, Martin LJ, Wong PC. "Motor neuron disease occurring in a mutant dynactin mouse model is characterized by defects in vasicular trafficking." J. Neurosci. 2008 Feb 27;28(9):1997-2005. doi: 10.1523/JNEUROSCI.4231-07.2008.
Martin LJ, Price AC, McClendon KB, Al-Abdulla NA, Subramaniam JR, Wong PC and Liu Z. "Early events of target deprivation/axotomy-induced neuronal apoptosis in vivo: oxidative stress, DNA damage, p53 phosphorylation and subcellular redistribution of death proteins." J Neurochem. 2003 Apr;85(1):234-47.
Martin LJ and Wong M. Aberrant regulation of DNA methylation in amyotrophic lateral sclerosis: A new target of disease mechanisms. Neurotherapeutics 10: 722-733, 2013.
Wong M, Gertz B, Chestnut BA and Martin LJ. Mitochondrial DNMT3A and DNA methylation in skeletal muscle and CNS of transgenic mouse models of ALS. Front. Cell. Neurosci. Dec 25;7:279. doi: 10.3389/fncel.2013.00279, 2013.
Martin LJ, Semenkow S, Hanaford A and Wong M. The mitochondrial permeability transition pore regulates Parkinson's disease development in mutant α-synuclein transgenic mice. Neurobiol. Aging 35:1132-1152, 2014.
Fayzullina A and Martin LJ. Skeletal muscle DNA damage precedes spinal motor neuron DNA damage in a mouse model of Spinal Muscular Atrophy (SMA). PLoS One. Mar 25;9(3):e93329. doi: 10.1371/journal.pone.0093329, 2014.
Martin LJ, Fancelli D, Wong M, Niedzwiecki M, Ballarini M, Plyte S and Chang Q. GNX-4728, a novel small molecule drug inhibitor of mitochondrial permeability transition, is therapeutic in a mouse model of amyotrophic lateral sclerosis. Front. Cell. Neurosci 8:433.doi: 10.3389/fncel.2014.00433, 2014.