Research Topics
Species | SERGE E PRZEDBORSKISummaryAffiliation: Columbia University Country: USA Publications
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Publications
Role of neuronal nitric oxide in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced dopaminergic neurotoxicityS Przedborski
Department of Neurology, Columbia University, New York 10032, USA
Proc Natl Acad Sci U S A 93:4565-71. 1996..These results indicate that neuronally derived NO mediates, in part, MPTP-induced neurotoxicity. The similarity between the MPTP model and PD raises the possibility that NO may play a significant role in the etiology of PD...- Molecular targets for neuroprotectionSerge Przedborski
Departments of Neurology and Pathology, and the Center for Neurobiology and Behavior, Columbia University, New York, NY 10032, USA
Amyotroph Lateral Scler Other Motor Neuron Disord 5:14-8. 2004..Information generated by these pre-clinical studies holds the promise to provide sound scientific basis for the development of effective neuroprotective therapies for ALS... - Programmed cell death in amyotrophic lateral sclerosis: a mechanism of pathogenic and therapeutic importanceSerge Przedborski
Department of Neurology, Center of Neurobiology and Behavior, Columbia University, New York, NY, USA
Neurologist 10:1-7. 2004..PCD, rather than being passive, is an active mechanism of cell death tightly regulated by multiple molecular pathways... - Pathogenesis of nigral cell death in Parkinson's diseaseSerge Przedborski
Departmentsof Neurology, Center for Neurobiology and Behavior, Columbia University, New York, NY 10032, USA
Parkinsonism Relat Disord 11:S3-7. 2005.... - The 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model: a tool to explore the pathogenesis of Parkinson's diseaseSerge Przedborski
Neuroscience Research Laboratories of the Movement Disorder Division, Department of Neurology, Columbia University, New York, New York 10032, USA
Ann N Y Acad Sci 991:189-98. 2003..How to target these factors to devise effective neuroprotective therapies for PD is also discussed... - MPTP as a mitochondrial neurotoxic model of Parkinson's diseaseSerge Przedborski
Department of Neurology, Columbia University, New York, New York 10032, USA
J Bioenerg Biomembr 36:375-9. 2004..How mitochondria are affected by MPTP and how their defect contributes to the demise of dopaminergic neurons in this model of PD are discussed in this review... - Neurodegeneration: what is it and where are we?Serge Przedborski
Department of Neurology, Columbia University, New York, New York 10032, USA
J Clin Invest 111:3-10. 2003 - Recent advances in amyotrophic lateral sclerosis researchSerge Przedborski
Department of Neurology, Columbia University College of Physicians and Surgeons, 650 West 168th Street, BB 307, New York, NY 10032, USA
Curr Neurol Neurosci Rep 3:70-7. 2003.... - Inflammation and Parkinson's disease pathogenesisSerge Przedborski
Department of Neurology, Pathology and Cell Biology, Columbia University, New York, New York, USA
Mov Disord 25:S55-7. 2010..Therapeutic strategies geared toward reducing inflammation and inhibiting the production of these glial-derived toxic molecules may be a promising neuroprotective strategy for the treatment of Parkinson's disease and related conditions... - Experimental developments in movement disorders: update on proposed free radical mechanismsS Przedborski
Department of Neurology, Columbia University, New York, NY 10032, USA
Curr Opin Neurol 11:335-9. 1998..Finally, the degree to which toxin-induced and genetically engineered experimental models have been useful in delineating parts of the mechanisms involved in the cascade of events that lead to neuronal death is emphasized... - Oxidative post-translational modifications of alpha-synuclein in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's diseaseS Przedborski
Department of Neurology, Columbia University, New York, NY 10032, USA
J Neurochem 76:637-40. 2001.... - Reactive oxygen and nitrogen species: weapons of neuronal destruction in models of Parkinson's diseaseSerge Przedborski
Department of Neurology, Center for Neurobiology and Behavior, Columbia University, New York, NY 10032, USA
Antioxid Redox Signal 7:685-93. 2005..This approach also enabled us to describe how our understanding of the mechanism of actions of certain toxins has evolved over time, which is particularly striking in the case of the quatrogenarian neurotoxin, 6-hydroxydopamine... - D-beta-hydroxybutyrate rescues mitochondrial respiration and mitigates features of Parkinson diseaseKim Tieu
Department of Neurology, Columbia University, New York, New York, USA
J Clin Invest 112:892-901. 2003..Because of the safety record of ketone bodies in the treatment of epilepsy and their ability to penetrate the blood-brain barrier, DbetaHB may be a novel neuroprotective therapy for PD... - Ablation of the inflammatory enzyme myeloperoxidase mitigates features of Parkinson's disease in miceDong-Kug Choi
Department of Neurology, Columbia University, New York, New York 10032, USA
J Neurosci 25:6594-600. 2005..This study demonstrates that MPO participates in the MPTP neurotoxic process and suggests that inhibitors of MPO may provide a protective benefit in PD... - L-3-hydroxyacyl-CoA dehydrogenase II protects in a model of Parkinson's diseaseKim Tieu
Department of Neurology, Columbia University, New York, NY 10032, USA
Ann Neurol 56:51-60. 2004..This study demonstrates that HADH II/ABAD modulates MPTP neurotoxicity and suggests that HADH II/ABAD mimetics may provide protective benefit in the treatment of PD... - Astrocytes expressing ALS-linked mutated SOD1 release factors selectively toxic to motor neuronsMakiko Nagai
Department of Neurology, Columbia University, 710 West 168th Street, New York, New York 10032, USA
Nat Neurosci 10:615-22. 2007..Identification of the astrocyte-derived soluble factor(s) may have far-reaching implications for ALS from both a pathogenic and therapeutic standpoint... - Blockade of microglial activation is neuroprotective in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson diseaseD C Wu
Department of Neurology, Columbia University, New York, New York 10032, USA
J Neurosci 22:1763-71. 2002..This study demonstrates that microglial-related inflammatory events play a significant role in the MPTP neurotoxic process and suggests that minocycline may be a valuable neuroprotective agent for the treatment of PD... - Complex I deficiency primes Bax-dependent neuronal apoptosis through mitochondrial oxidative damageCeline Perier
Department of Neurology, Columbia University, New York, NY 10032, USA
Proc Natl Acad Sci U S A 102:19126-31. 2005..This molecular scenario may have far-reaching implications for the development of effective neuroprotective therapies for these incurable illnesses... - Mutant LRRK2(R1441G) BAC transgenic mice recapitulate cardinal features of Parkinson's diseaseYanping Li
Department of Neurology and Neurosciences, Weill Medical College of Cornell University, New York, New York, USA
Nat Neurosci 12:826-8. 2009..These mice provide a valid model of Parkinson's disease and are a resource for the investigation of pathogenesis and therapeutics... - NADPH oxidase mediates oxidative stress in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model of Parkinson's diseaseDu-Chu Wu
Department of Neurology, Columbia University, New York, NY 10032, USA
Proc Natl Acad Sci U S A 100:6145-50. 2003..This study supports a critical role for NADPH-oxidase in the pathogenesis of PD and suggests that targeting this enzyme or enhancing extracellular antioxidants may provide novel therapies for PD... - Pathogenic role of glial cells in Parkinson's diseasePeter Teismann
Neuroscience Research, Movement Disorder Division, Department of Neurology, Columbia University, New York, New York 10032, USA
Mov Disord 18:121-9. 2003..We discuss the potential protective and deleterious effects of glial cells in the SNpc of PD and examine how those factors may contribute to the pathogenesis of this disease... - The inflammatory NADPH oxidase enzyme modulates motor neuron degeneration in amyotrophic lateral sclerosis miceDu Chu Wu
Department of Neurology, Columbia University, New York, NY 10032, USA
Proc Natl Acad Sci U S A 103:12132-7. 2006..These findings suggest a non-cell-autonomous mechanism through which inflammation could hasten motor neuron death and contribute to the selective motor neuronal degeneration in ALS... - Genetic clues to the pathogenesis of Parkinson's diseaseMiquel Vila
Department of Neurology, Center for Neurobiology and Behavior, Columbia University, New York, New York 10032, USA
Nat Med 10:S58-62. 2004..These breakthroughs have not provided a direct explanation for the disease process. Nevertheless, they have helped transform Parkinson's disease research by providing tangible clues to the neurobiology of the disorder... - What can pluripotent stem cells teach us about neurodegenerative diseases?Hynek Wichterle
Department of Neurology, Columbia University, New York, New York, USA
Nat Neurosci 13:800-4. 2010..Progress in these four areas will substantially accelerate effective application of pluripotent stem cells... - Rapamycin protects against neuron death in in vitro and in vivo models of Parkinson's diseaseCristina Malagelada
Department of Pathology and Cell Biology, Columbia University, New York, New York 10032, USA
J Neurosci 30:1166-75. 2010.... - Free radical and nitric oxide toxicity in Parkinson's diseaseSerge Przedborski
Departments of Neurology and Pathology, Columbia University, New York, New York, USA
Adv Neurol 91:83-94. 2003 - Protocol for the MPTP mouse model of Parkinson's diseaseVernice Jackson Lewis
Department of Neurology, Columbia University, New York, NY 10032, USA
Nat Protoc 2:141-51. 2007..This protocol calls for implementation of safety measures and for the acquisition of several pieces of equipment, which are a one-time investment worth making if one elects to use this model on a regular basis... - Resistance of alpha -synuclein null mice to the parkinsonian neurotoxin MPTPWilliam Dauer
Department of Neurology, Columbia University, New York, NY 10027, USA
Proc Natl Acad Sci U S A 99:14524-9. 2002.... - Is prostaglandin E(2) a pathogenic factor in amyotrophic lateral sclerosis?Gabriele Almer
Department of Neurology, Columbia University, New York, NY 10032, USA
Ann Neurol 59:980-3. 2006..Furthermore, plans to use selective Cox-1 inhibitors for neuroprotection in ALS are unlikely to be fruitful... - Targeting programmed cell death in neurodegenerative diseasesMiquel Vila
Department of Neurology, Columbia University, 650 West 168th Street, BB-307, New York, New York 10032, USA
Nat Rev Neurosci 4:365-75. 2003 - CHOP/GADD153 is a mediator of apoptotic death in substantia nigra dopamine neurons in an in vivo neurotoxin model of parkinsonismRobert M Silva
Department of Neurology, The College of Physicians and Surgeons, Columbia University, New York 10032, USA
J Neurochem 95:974-86. 2005..We conclude that the role of CHOP depends on the nature of the toxic stimulus. For 6OHDA, an oxidative metabolite of dopamine, it is a mediator of apoptotic death... - Inflammation in ALS and SMA: sorting out the good from the evilDimitra Papadimitriou
Department of Neurology, New York, NY, USA
Neurobiol Dis 37:493-502. 2010..Herein, we will review neuroinflammation in both ALS and SMA not only from the angle of neuropathology but also from the angle of its potential role in the pathogenesis and treatment of these two dreadful paralytic disorders... - Is there a pathogenic role for mitochondria in Parkinson's disease?Cristofol Vives-Bauza
Department of Neurology, Columbia University, New York, New York 10032, USA
Parkinsonism Relat Disord 15:S241-4. 2009.... - Transgenic superoxide dismutase overproducer: murineSerge Przedborski
Departments of Neurology and Pathology, Columbia University, New York, New York 10032, USA
Methods Enzymol 349:180-90. 2002 - Cyclooxygenase-2 is instrumental in Parkinson's disease neurodegenerationPeter Teismann
Neuroscience Research Laboratories of the Movement Disorder Division, Department of Neurology, Columbia University, New York, NY 10032, USA
Proc Natl Acad Sci U S A 100:5473-8. 2003..Because of the safety record of the COX-2 inhibitors, and their ability to penetrate the blood-brain barrier, these drugs may be therapies for PD... - Nitric oxide and reactive oxygen species in Parkinson's diseaseKim Tieu
Department of Neurology, Columbia University, New York, NY 10032, USA
IUBMB Life 55:329-35. 2003..Similar contribution of reactive nitrogen and oxygen species may well underlie the neurodegenerative processes in Parkinson's disease... - Parkinson's disease: mechanisms and modelsWilliam Dauer
Department of Neurology, Columbia University, New York, NY 10032, USA
Neuron 39:889-909. 2003..PD models based on the manipulation of PD genes should prove valuable in elucidating important aspects of the disease, such as selective vulnerability of substantia nigra dopaminergic neurons to the degenerative process... - Dopamine-modified alpha-synuclein blocks chaperone-mediated autophagyMarta Martinez-Vicente
Department of Anatomy and Structural Biology, Albert Einstein College of Medicine, Yeshiva University, New York, New York 10461, USA
J Clin Invest 118:777-88. 2008..As blockage of CMA increases cellular vulnerability to stressors, we propose that dopamine-induced autophagic inhibition could explain the selective degeneration of PD dopaminergic neurons... - Spinal cord endoplasmic reticulum stress associated with a microsomal accumulation of mutant superoxide dismutase-1 in an ALS modelHitoshi Kikuchi
Department of Neurology, Columbia University, New York, NY 10032, USA
Proc Natl Acad Sci U S A 103:6025-30. 2006..Our results suggest a toxic mechanism for mutant SOD1 by which this ubiquitously expressed pathogenic protein could affect motor neuron survival and contribute to the selective motor neuronal degeneration in ALS... - Control of mitochondrial integrity in Parkinson's diseaseCristofol Vives-Bauza
Department of Neurology, Motor Neuron Biology and Disease, Columbia University, New York, NY, USA
Prog Brain Res 183:99-113. 2010.... - Alpha-synuclein overexpression increases cytosolic catecholamine concentrationEugene V Mosharov
Department of Neurology, Columbia University Medical Center, New York, New York 10032, USA
J Neurosci 26:9304-11. 2006.... - The kinase domain of mitochondrial PINK1 faces the cytoplasmChun Zhou
Department of Neurology, Columbia University, 650 West 168th Street, New York, NY 10032, USA
Proc Natl Acad Sci U S A 105:12022-7. 2008..These results are critical in rectifying the location and orientation of PINK1 in mitochondria, and they should help decipher its normal physiological function and potential pathogenic role in PD... - PINK1-dependent recruitment of Parkin to mitochondria in mitophagyCristofol Vives-Bauza
Department of Neurology, Columbia University, New York, NY 10032, USA
Proc Natl Acad Sci U S A 107:378-83. 2010..Thus by impairing this process, mutations in either Parkin or PINK1 may alter mitochondrial turnover which, in turn, may cause the accumulation of defective mitochondria and, ultimately, neurodegeneration in Parkinson's disease... - Prion protein codon 129 genotype prevalence is altered in primary progressive aphasiaXiaohong Li
Department of Neurology, Pritzker School of Medicine and Center for Comprehensive Care and Research on Memory Disorders, University of Chicago, 5841 S Maryland Avenue, Chicago, IL 60637, USA
Ann Neurol 58:858-64. 2005..However, the strong association between heterozygosity and PPA raises new questions about its cause and the role of PrP in other neurodegenerative diseases... - Glial cell response: A pathogenic factor in Parkinson's diseaseDu Chu Wu
Neuroscience Research, Movement Disorder Division, Department of Neurology, Columbia University, New York, New York, USA
J Neurovirol 8:551-8. 2002..In this review, the authors discuss the potential protective and deleterious effects of glial cells in the SNpc of PD and examine how these factors may contribute to the pathogenesis of this disease... - Oxidative stress in Parkinson's disease: a mechanism of pathogenic and therapeutic significanceChun Zhou
Department of Neurology, Columbia University, New York, NY 10032, USA
Ann N Y Acad Sci 1147:93-104. 2008..If correct, this may be a reason why neuroprotective trials using a single agent, such as an antioxidant, have thus far generated disappointing results... - A sequel to the tale of p25/Cdk5 in neurodegenerationBurcin Ikiz
Department of Neurology, Pathology, and Cell Biology and Center for Motor Neuron Biology and Disease, Columbia University, New York, NY 10032, USA
Neuron 60:731-2. 2008..This study provides further insights into the function of p25/Cdk5 in neurons and points to HDAC-1 as a target for therapeutic interventions... - Intrabody and Parkinson's diseaseChun Zhou
Department of Neurology, Columbia University, New York, NY 10032, USA
Biochim Biophys Acta 1792:634-42. 2009..Furthermore, we propose possible intrabody applications against leucine-rich repeat kinase 2 (LRRK2), whose mutations are the most frequent known cause of familial and sporadic PD...
Research Grants
- Proinflammatory enzymes in amytrophic lateral sclerosisSerge Przedborski; Fiscal Year: 2009..Herein, we propose to; search for this toxic factor; to demonstrate by which mechanism it kills cells; and to demonstrate whether a similar situation occurs in an animal model of ALS. ..
- Mechanisms of Bax-mediated cell death in the MPTP modelSerge Przedborski; Fiscal Year: 2007..Collectively, the proposed studies should shed light on the molecular mechanisms of neurodegeneration in PD and help to identify new molecular targets for therapeutic intervention. ..
- Effect of enriched environment on ALS neurodegenerationSerge Przedborski; Fiscal Year: 2005..This development/exploratory project offers an high-risk/high-yield set of studies which may demonstrate, in an original way, how environment may impact on the occurrence and the progression of ALS. ..
- Proinflammatory enzymes in amyotrophic lateral sclerosisSerge Przedborski; Fiscal Year: 2004..It should also shed light onto the mechanisms of neurodegeneration in ALS. ..
- SYNUCLEIN AND NIGRAL DOPAMINERGIC NEURON DEGENERATIONSerge Przedborski; Fiscal Year: 2003....
- NITRIC OXIDE AND PROTEIN NITROTYROSINE IN THE MPTP MODELSerge Przedborski; Fiscal Year: 2002..This proposal contains a comprehensive set of experiments, which should provide important insights into the role of NO in MPTP toxicity. It should also shed light on the mechanism(s) of neurodegeneration in PD. ..
- Proinflammatory enzymes in amytrophic lateral sclerosisSERGE E PRZEDBORSKI; Fiscal Year: 2010..Herein, we propose to;search for this toxic factor;to demonstrate by which mechanism it kills cells;and to demonstrate whether a similar situation occurs in an animal model of ALS. ..