Timothy M Miller

Summary

Affiliation: University of California
Country: USA

Publications

  1. ncbi request reprint Proposed modification to data analysis for statistical motor unit number estimate
    Timothy M Miller
    Department of Neurology, University of California San Francisco, San Francisco, California, USA
    Muscle Nerve 29:700-6. 2004
  2. ncbi request reprint Muscle cramps
    Timothy M Miller
    Department of Neurosciences, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093 0670, USA
    Muscle Nerve 32:431-42. 2005
  3. pmc Gene transfer demonstrates that muscle is not a primary target for non-cell-autonomous toxicity in familial amyotrophic lateral sclerosis
    Timothy M Miller
    Ludwig Institute for Cancer Research, La Jolla, CA 92093, USA
    Proc Natl Acad Sci U S A 103:19546-51. 2006
  4. ncbi request reprint Amyotrophic lateral sclerosis and gene therapy
    Timothy M Miller
    Department of Neurosciences, Ludwig Institute for Cancer Research, University of California, San Diego, La Jolla, CA 92093 0670, USA
    Nat Clin Pract Neurol 2:462-3. 2006
  5. pmc ALS-linked mutant superoxide dismutase 1 (SOD1) alters mitochondrial protein composition and decreases protein import
    Quan Li
    Department of Neurology, Hope Center for Neurological Disorders, The Washington University School of Medicine, St Louis, MO 63110, USA
    Proc Natl Acad Sci U S A 107:21146-51. 2010
  6. pmc Selective association of misfolded ALS-linked mutant SOD1 with the cytoplasmic face of mitochondria
    Christine Vande Velde
    Ludwig Institute and Departments of Medicine and Neuroscience, University of California at San Diego, 9500 Gilman Drive, La Jolla, CA 92093 0670, USA
    Proc Natl Acad Sci U S A 105:4022-7. 2008
  7. ncbi request reprint Progressive spinal axonal degeneration and slowness in ALS2-deficient mice
    Koji Yamanaka
    Ludwig Institute for Cancer Research and Department of Medicine and Neurosciences, University of California, San Diego, La Jolla, 92093 0670, USA
    Ann Neurol 60:95-104. 2006
  8. pmc Antisense oligonucleotide therapy for neurodegenerative disease
    Richard A Smith
    Ludwig Institute for Cancer Research, University of California, San Diego, La Jolla, California, USA
    J Clin Invest 116:2290-6. 2006
  9. doi request reprint Familial ALS with extreme phenotypic variability due to the I113T SOD1 mutation
    Glenn Lopate
    Washington University School of Medicine, Department of Neurology, Saint Louis, Missouri 63110, USA
    Amyotroph Lateral Scler 11:232-6. 2010
  10. doi request reprint Gene-targeted therapies for the central nervous system
    Timothy M Miller
    Neurosciences Department, University of California, San Diego, San Diego, California, USA
    Arch Neurol 65:447-51. 2008

Collaborators

Detail Information

Publications23

  1. ncbi request reprint Proposed modification to data analysis for statistical motor unit number estimate
    Timothy M Miller
    Department of Neurology, University of California San Francisco, San Francisco, California, USA
    Muscle Nerve 29:700-6. 2004
    ....
  2. ncbi request reprint Muscle cramps
    Timothy M Miller
    Department of Neurosciences, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093 0670, USA
    Muscle Nerve 32:431-42. 2005
    ..Patients will benefit from further studies to better define the pathophysiology of muscle cramps and to find more effective medications with fewer side-effects...
  3. pmc Gene transfer demonstrates that muscle is not a primary target for non-cell-autonomous toxicity in familial amyotrophic lateral sclerosis
    Timothy M Miller
    Ludwig Institute for Cancer Research, La Jolla, CA 92093, USA
    Proc Natl Acad Sci U S A 103:19546-51. 2006
    ..Thus, SOD1-mutant-mediated damage within muscles is not a significant contributor to non-cell-autonomous pathogenesis in ALS, and enhancing muscle mass and strength provides no benefit in slowing disease onset or progression...
  4. ncbi request reprint Amyotrophic lateral sclerosis and gene therapy
    Timothy M Miller
    Department of Neurosciences, Ludwig Institute for Cancer Research, University of California, San Diego, La Jolla, CA 92093 0670, USA
    Nat Clin Pract Neurol 2:462-3. 2006
  5. pmc ALS-linked mutant superoxide dismutase 1 (SOD1) alters mitochondrial protein composition and decreases protein import
    Quan Li
    Department of Neurology, Hope Center for Neurological Disorders, The Washington University School of Medicine, St Louis, MO 63110, USA
    Proc Natl Acad Sci U S A 107:21146-51. 2010
    ..Thus, altered mitochondrial protein content accompanied by selective decreases in protein import into spinal cord mitochondria comprises part of the mitochondrial damage arising from mutant SOD1...
  6. pmc Selective association of misfolded ALS-linked mutant SOD1 with the cytoplasmic face of mitochondria
    Christine Vande Velde
    Ludwig Institute and Departments of Medicine and Neuroscience, University of California at San Diego, 9500 Gilman Drive, La Jolla, CA 92093 0670, USA
    Proc Natl Acad Sci U S A 105:4022-7. 2008
    ....
  7. ncbi request reprint Progressive spinal axonal degeneration and slowness in ALS2-deficient mice
    Koji Yamanaka
    Ludwig Institute for Cancer Research and Department of Medicine and Neurosciences, University of California, San Diego, La Jolla, 92093 0670, USA
    Ann Neurol 60:95-104. 2006
    ..The goal of this study was to elucidate how the motor system is affected by the deletion of ALS2...
  8. pmc Antisense oligonucleotide therapy for neurodegenerative disease
    Richard A Smith
    Ludwig Institute for Cancer Research, University of California, San Diego, La Jolla, California, USA
    J Clin Invest 116:2290-6. 2006
    ..This suggests that direct delivery of antisense oligonucleotides could be an effective, dosage-regulatable means of treating neurodegenerative diseases, including ALS, where appropriate target proteins are known...
  9. doi request reprint Familial ALS with extreme phenotypic variability due to the I113T SOD1 mutation
    Glenn Lopate
    Washington University School of Medicine, Department of Neurology, Saint Louis, Missouri 63110, USA
    Amyotroph Lateral Scler 11:232-6. 2010
    ..This family highlights the extreme variability in age of onset, clinical manifestations, disease progression and penetrance due to the I113T SOD1 mutation...
  10. doi request reprint Gene-targeted therapies for the central nervous system
    Timothy M Miller
    Neurosciences Department, University of California, San Diego, San Diego, California, USA
    Arch Neurol 65:447-51. 2008
  11. pmc Canine degenerative myelopathy: biochemical characterization of superoxide dismutase 1 in the first naturally occurring non-human amyotrophic lateral sclerosis model
    Matthew J Crisp
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Exp Neurol 248:1-9. 2013
    ..Our findings lend strong biochemical support to the toxic role of SOD1 in canine degenerative myelopathy and establish close parallels for the role mutant SOD1 plays in both canine and human disorders. ..
  12. pmc SOD1 in cerebral spinal fluid as a pharmacodynamic marker for antisense oligonucleotide therapy
    Leah Winer
    Department of Neurology, Washington University, St Louis, Missouri 63110, USA
    JAMA Neurol 70:201-7. 2013
    ..Therapies designed to decrease the level of SOD1 are currently in a clinical trial for patients with superoxide dismutase (SOD1)-linked familial amyotrophic lateral sclerosis (ALS)...
  13. pmc Virus-delivered small RNA silencing sustains strength in amyotrophic lateral sclerosis
    Timothy M Miller
    Ludwig Institute for Cancer Research, University of California, San Diego, USA
    Ann Neurol 57:773-6. 2005
    ....
  14. ncbi request reprint Toxicity of familial ALS-linked SOD1 mutants from selective recruitment to spinal mitochondria
    Jian Liu
    Ludwig Institute for Cancer Research, Department of Neurosciences, Medicine, and Cellular and Molecular Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA
    Neuron 43:5-17. 2004
    ..These findings implicate damage from action of spinal cord-specific factors that recruit mutant SOD1 to spinal mitochondria as the basis for their selective toxicity in ALS...
  15. pmc RCADiA: simple automation platform for comparative multidimensional protein identification technology
    Aaron O Bailey
    Department of Cell Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, SR11, La Jolla, California 92037, USA
    Anal Chem 79:6410-8. 2007
    ..We demonstrate this device by performing a comparative analysis of mitochondria enriched from rat liver and spinal cord...
  16. ncbi request reprint Should the Babinski sign be part of the routine neurologic examination?
    Timothy M Miller
    Department of Neurology, University of California, San Francisco, CA, USA
    Neurology 65:1165-8. 2005
    ..A less well-known sign of upper motor neuron dysfunction, decreased speed of foot tapping, also has not been carefully evaluated. Scientific evaluation of findings of the physical examination is crucial in directing busy clinicians...
  17. pmc Heparan sulfate proteoglycans mediate internalization and propagation of specific proteopathic seeds
    Brandon B Holmes
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Proc Natl Acad Sci U S A 110:E3138-47. 2013
    ..Finally, uptake and seeding by α-synuclein fibrils, but not huntingtin fibrils, occurs by the same mechanism as tau. This work suggests a unifying mechanism of cell uptake and propagation for tauopathy and synucleinopathy. ..
  18. pmc Antisense oligonucleotides: treating neurodegeneration at the level of RNA
    Sarah L DeVos
    Department of Neurology, Washington University in St Louis School of Medicine, St Louis, MO 63110, USA
    Neurotherapeutics 10:486-97. 2013
    ..Although still early in development, translating ASOs into human patients for neurodegeneration appears promising. ..
  19. pmc Antisense reduction of tau in adult mice protects against seizures
    Sarah L DeVos
    Department of Neurology, Hope Center for Neurological Disorders, Washington University, St Louis, Missouri 63110, USA
    J Neurosci 33:12887-97. 2013
    ....
  20. ncbi request reprint Medicine. Treating neurodegenerative diseases with antibiotics
    Timothy M Miller
    Ludwig Institute for Cancer Research and the Department of Medicine and Neurosciences, University of California, San Diego, La Jolla, CA 92093, USA
    Science 307:361-2. 2005
  21. ncbi request reprint Unraveling the mechanisms involved in motor neuron degeneration in ALS
    Lucie I Bruijn
    ALS Association, Guilford, Connecticut 06437, USA
    Annu Rev Neurosci 27:723-49. 2004
    ....
  22. ncbi request reprint Has gene therapy for ALS arrived?
    Timothy M Miller
    Nat Med 9:1256-7. 2003
  23. ncbi request reprint Differential diagnosis of myotonic disorders
    Timothy M Miller
    Neurology Department, Washington University, St Louis, MI, USA
    Muscle Nerve 37:293-9. 2008
    ..Acid maltase deficiency often produces myotonic potentials without clinical evidence of myotonia or paramyotonia. The differential diagnosis of these myotonic disorders is discussed...