Mitochondrial dysfunction as a cause of axonal degeneration in multiple sclerosis patients

Degeneration of chronically demyelinated axons is a major cause of irreversible neurological disability in multiple sclerosis (MS) patients. Development of neuroprotective therapies will require elucidation of the molecular mechanisms by which neurons and axons degenerate.

[1]  Peter K. Stys,et al.  General mechanisms of axonal damage and its prevention , 2005, Journal of the Neurological Sciences.

[2]  Ilana S. Hairston,et al.  Environmental Enrichment Reduces Aβ Levels and Amyloid Deposition in Transgenic Mice , 2005, Cell.

[3]  K. Mirnics,et al.  Presenilin-1-Dependent Transcriptome Changes , 2005, The Journal of Neuroscience.

[4]  Stephen G Waxman,et al.  Na+ channel expression along axons in multiple sclerosis and its models. , 2004, Trends in pharmacological sciences.

[5]  J. Wilusz,et al.  Bringing the role of mRNA decay in the control of gene expression into focus. , 2004, Trends in genetics : TIG.

[6]  A. Lo,et al.  Sodium channel blockade with phenytoin protects spinal cord axons, enhances axonal conduction, and improves functional motor recovery after contusion SCI , 2004, Experimental Neurology.

[7]  Ludwig Kappos,et al.  Multiple sclerosis as a generalized CNS disease—comparative microarray analysis of normal appearing white matter and lesions in secondary progressive MS , 2004, Journal of Neuroimmunology.

[8]  Jia Newcombe,et al.  Molecular changes in neurons in multiple sclerosis: altered axonal expression of Nav1.2 and Nav1.6 sodium channels and Na+/Ca2+ exchanger. , 2004, Proceedings of the National Academy of Sciences of the United States of America.

[9]  D. Bechtold,et al.  Axonal protection using flecainide in experimental autoimmune encephalomyelitis , 2004, Annals of neurology.

[10]  Michael A. Beer,et al.  Predicting Gene Expression from Sequence , 2004, Cell.

[11]  P. Stys White matter injury mechanisms. , 2004, Current molecular medicine.

[12]  F. Zipp,et al.  Activation of Microglial Poly(ADP-Ribose)-Polymerase-1 by Cholesterol Breakdown Products during Neuroinflammation , 2003, The Journal of experimental medicine.

[13]  L. Griffiths,et al.  Quantitative and qualitative changes in gene expression patterns characterize the activity of plaques in multiple sclerosis. , 2003, Brain research. Molecular brain research.

[14]  R. Reynolds,et al.  Molecular Changes in Normal Appearing White Matter in Multiple Sclerosis are Characteristic of Neuroprotective Mechanisms Against Hypoxic Insult , 2003, Brain pathology.

[15]  Douglas A. Hosack,et al.  Identifying biological themes within lists of genes with EASE , 2003, Genome Biology.

[16]  A. Sampson,et al.  Gene Expression Deficits in a Subclass of GABA Neurons in the Prefrontal Cortex of Subjects with Schizophrenia , 2003, The Journal of Neuroscience.

[17]  J. Fritschy,et al.  Formation and plasticity of GABAergic synapses: physiological mechanisms and pathophysiological implications. , 2003, Pharmacology & therapeutics.

[18]  Rafael A Irizarry,et al.  Exploration, normalization, and summaries of high density oligonucleotide array probe level data. , 2003, Biostatistics.

[19]  M. Brunori,et al.  Nitric oxide and cytochrome oxidase: reaction mechanisms from the enzyme to the cell. , 2003, Free radical biology & medicine.

[20]  Kenneth J. Smith,et al.  Blockers of sodium and calcium entry protect axons from nitric oxide‐mediated degeneration , 2003, Annals of neurology.

[21]  H. Bading,et al.  The Yin and Yang of NMDA receptor signalling , 2003, Trends in Neurosciences.

[22]  Ulf Ziemann,et al.  Rapid modulation of GABA in sensorimotor cortex induced by acute deafferentation , 2002, Annals of neurology.

[23]  W. Sieghart,et al.  Homologous sites of GABAA receptor α1, β3 and γ2 subunits are important for assembly , 2002, Neuropharmacology.

[24]  P. Stys,et al.  Calpain-dependent neurofilament breakdown in anoxic and ischemic rat central axons , 2002, Neuroscience Letters.

[25]  H. Bading,et al.  Extrasynaptic NMDARs oppose synaptic NMDARs by triggering CREB shut-off and cell death pathways , 2002, Nature Neuroscience.

[26]  Jorge R. Oksenberg,et al.  Gene-microarray analysis of multiple sclerosis lesions yields new targets validated in autoimmune encephalomyelitis , 2002, Nature Medicine.

[27]  W. Sieghart,et al.  Homologous sites of GABA(A) receptor alpha(1), beta(3) and gamma(2) subunits are important for assembly. , 2002, Neuropharmacology.

[28]  Jason E. Stewart,et al.  Minimum information about a microarray experiment (MIAME)—toward standards for microarray data , 2001, Nature Genetics.

[29]  B. Trapp,et al.  Transected neurites, apoptotic neurons, and reduced inflammation in cortical multiple sclerosis lesions , 2001, Annals of neurology.

[30]  D. Colman,et al.  Organizing Principles of the Axoglial Apparatus , 2001, Neuron.

[31]  B. J. Hanson,et al.  Human Complex I Defects Can Be Resolved by Monoclonal Antibody Analysis into Distinct Subunit Assembly Patterns* , 2001, The Journal of Biological Chemistry.

[32]  D. Turnbull,et al.  Assaying mitochondrial respiratory complex activity in mitochondria isolated from human cells and tissues. , 2001, Methods in cell biology.

[33]  R. Rudick,et al.  Neurological disability correlates with spinal cord axonal loss and reduced N‐acetyl aspartate in chronic multiple sclerosis patients , 2000, Annals of neurology.

[34]  Adelbert Ames,et al.  CNS energy metabolism as related to function , 2000, Brain Research Reviews.

[35]  Pat Levitt,et al.  Molecular Characterization of Schizophrenia Viewed by Microarray Analysis of Gene Expression in Prefrontal Cortex , 2000, Neuron.

[36]  S. Croul,et al.  Oxidative damage to mitochondrial DNA and activity of mitochondrial enzymes in chronic active lesions of multiple sclerosis , 2000, Journal of the Neurological Sciences.

[37]  P. Stys,et al.  Calpain Inhibitors Confer Biochemical, but Not Electrophysiological, Protection Against Anoxia in Rat Optic Nerves , 2000, Journal of neurochemistry.

[38]  M. Blinkenberg,et al.  Cortical cerebral metabolism correlates with MRI lesion load and cognitive dysfunction in MS , 2000, Neurology.

[39]  J. Trent,et al.  Analysis of gene expression in multiple sclerosis lesions using cDNA microarrays , 1999 .

[40]  R. Herndon,et al.  Selecting relapsing remitting multiple sclerosis patients for treatment: the case for early treatment , 1999, Journal of Neuroimmunology.

[41]  N. Brandon,et al.  GABAA-receptor-associated protein links GABAA receptors and the cytoskeleton , 1999, Nature.

[42]  R. Rudick,et al.  Neurodegeneration in Multiple Sclerosis: Relationship to Neurological Disability , 1999 .

[43]  R. Rudick,et al.  Axonal transection in the lesions of multiple sclerosis. , 1998, The New England journal of medicine.

[44]  E. Salmon,et al.  How calcium causes microtubule depolymerization. , 1997, Cell motility and the cytoskeleton.

[45]  T. Dawson,et al.  Neurobiology of nitric oxide. , 1996, Critical reviews in neurobiology.

[46]  M. Wong-Riley,et al.  Disproportionate regulation of nuclear- and mitochondrial-encoded cytochrome oxidase subunit proteins by functional activity in neurons , 1995, Neuroscience.

[47]  G. Kreutzberg,et al.  Microglia: Intrinsic immuneffector cell of the brain , 1995, Brain Research Reviews.

[48]  C. Hoppel,et al.  Decreased activities of ubiquinol:ferricytochrome c oxidoreductase (complex III) and ferrocytochrome c:oxygen oxidoreductase (complex IV) in liver mitochondria from rats with hydroxycobalamin[c-lactam]-induced methylmalonic aciduria. , 1991, The Journal of biological chemistry.

[49]  S. Waxman,et al.  Na+‐Ca2+ exchanger mediates Ca2+ influx during anoxia in mammalian central nervous system white matter , 1991, Annals of neurology.

[50]  E. G. Jones,et al.  Numbers and proportions of GABA-immunoreactive neurons in different areas of monkey cerebral cortex , 1987, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[51]  W. L. Benedict,et al.  Multiple Sclerosis , 2007, Journal - Michigan State Medical Society.