A Pestronk

Summary

Affiliation: Washington University School of Medicine
Country: USA

Publications

  1. ncbi request reprint Serum antibodies to heparan sulfate glycosaminoglycans in Guillain-Barré syndrome and other demyelinating polyneuropathies
    A Pestronk
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    J Neuroimmunol 91:204-9. 1998
  2. pmc Treatment of IgM antibody associated polyneuropathies using rituximab
    A Pestronk
    Department of Neurology, Box 8111, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA
    J Neurol Neurosurg Psychiatry 74:485-9. 2003
  3. ncbi request reprint Sensory neuropathy with monoclonal IgM binding to a trisulfated heparin disaccharide
    Alan Pestronk
    Washington University School of Medicine, Department of Neurology, Box 8111, 660 South Euclid Ave, St Louis, MO 63110, USA
    Muscle Nerve 27:188-95. 2003
  4. ncbi request reprint Sensory exam with a quantitative tuning fork: rapid, sensitive and predictive of SNAP amplitude
    A Pestronk
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Neurology 62:461-4. 2004
  5. ncbi request reprint Inflammatory and immune myopathies: concepts in diagnosis and treatment
    Alan Pestronk
    Department of Neurology, Washington University School of Medicine, St Louis, MO, USA
    J Child Neurol 17:205. 2002
  6. ncbi request reprint Anti-myelin associated glycoprotein antibodies: variability in patterns of IgM binding to peripheral nerve
    G Lopate
    Department of Neurology, Washington University School of Medicine, Box 8111, 660 S. Euclid Ave, St. Louis, MO 63110, USA
    J Neurol Sci 188:67-72. 2001
  7. pmc Myopathy with antibodies to the signal recognition particle: clinical and pathological features
    T Miller
    Washington University School of Medicine, Department of Neurology, St Louis, Missouri 63110, USA
    J Neurol Neurosurg Psychiatry 73:420-8. 2002
  8. pmc TDP-43 A315T mutation in familial motor neuron disease
    Michael A Gitcho
    Alzheimer s Disease Research Center, Washington University School of Medicine, St Louis, MO 63110, USA
    Ann Neurol 63:535-8. 2008
  9. doi request reprint High aldolase with normal creatine kinase in serum predicts a myopathy with perimysial pathology
    K Nozaki
    Washington University School of Medicine, Department of Neurology, 660 South Euclid Ave, St Louis, MO 63110, USA
    J Neurol Neurosurg Psychiatry 80:904-8. 2009
  10. ncbi request reprint Anti-sulfatide antibodies in HIV-infected individuals with sensory neuropathy
    G Lopate
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Neurology 64:1632-4. 2005

Detail Information

Publications52

  1. ncbi request reprint Serum antibodies to heparan sulfate glycosaminoglycans in Guillain-Barré syndrome and other demyelinating polyneuropathies
    A Pestronk
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    J Neuroimmunol 91:204-9. 1998
    ....
  2. pmc Treatment of IgM antibody associated polyneuropathies using rituximab
    A Pestronk
    Department of Neurology, Box 8111, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA
    J Neurol Neurosurg Psychiatry 74:485-9. 2003
    ..This study tested the ability of rituximab to produce changes in serum antibody titres, and improvement in strength, in patients with neuromuscular disorders and IgM autoantibodies...
  3. ncbi request reprint Sensory neuropathy with monoclonal IgM binding to a trisulfated heparin disaccharide
    Alan Pestronk
    Washington University School of Medicine, Department of Neurology, Box 8111, 660 South Euclid Ave, St Louis, MO 63110, USA
    Muscle Nerve 27:188-95. 2003
    ..The role of IgM binding to TS-HDS in the pathogenesis of the neuropathy remains to be determined...
  4. ncbi request reprint Sensory exam with a quantitative tuning fork: rapid, sensitive and predictive of SNAP amplitude
    A Pestronk
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Neurology 62:461-4. 2004
    ....
  5. ncbi request reprint Inflammatory and immune myopathies: concepts in diagnosis and treatment
    Alan Pestronk
    Department of Neurology, Washington University School of Medicine, St Louis, MO, USA
    J Child Neurol 17:205. 2002
  6. ncbi request reprint Anti-myelin associated glycoprotein antibodies: variability in patterns of IgM binding to peripheral nerve
    G Lopate
    Department of Neurology, Washington University School of Medicine, Box 8111, 660 S. Euclid Ave, St. Louis, MO 63110, USA
    J Neurol Sci 188:67-72. 2001
    ..These different binding patterns may relate to the ability of anti-MAG serum IgM to bind both MAG and SGPG or to other molecules with a sulfated glucuronic acid epitope that are present in peripheral nerve...
  7. pmc Myopathy with antibodies to the signal recognition particle: clinical and pathological features
    T Miller
    Washington University School of Medicine, Department of Neurology, St Louis, Missouri 63110, USA
    J Neurol Neurosurg Psychiatry 73:420-8. 2002
    ..To study myopathies with serum antibodies to the signal recognition particle (SRP), an unusual, myositis specific antibody associated syndrome that has not been well characterised pathologically...
  8. pmc TDP-43 A315T mutation in familial motor neuron disease
    Michael A Gitcho
    Alzheimer s Disease Research Center, Washington University School of Medicine, St Louis, MO 63110, USA
    Ann Neurol 63:535-8. 2008
    ..The discovery of a missense mutation in TDP-43 in a family with dominantly inherited motor neuron disease provides evidence of a direct link between altered TDP-43 function and neurodegeneration...
  9. doi request reprint High aldolase with normal creatine kinase in serum predicts a myopathy with perimysial pathology
    K Nozaki
    Washington University School of Medicine, Department of Neurology, 660 South Euclid Ave, St Louis, MO 63110, USA
    J Neurol Neurosurg Psychiatry 80:904-8. 2009
    ..To study the clinical and pathological correlations of neuromuscular patients with a high aldolase and normal creatine kinase (CK) in serum at presentation or during a symptomatic exacerbation...
  10. ncbi request reprint Anti-sulfatide antibodies in HIV-infected individuals with sensory neuropathy
    G Lopate
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Neurology 64:1632-4. 2005
    ..We found that 36% of HIV+/DSP+ individuals had immunoglobulin (Ig) G anti-sulfatide antibody titers greater than 1,500, whereas IgG anti-sulfatide antibodies were rarely found in HIV+/DSP- or HIV-/DSP+ patients...
  11. ncbi request reprint Three mouse models of muscular dystrophy: the natural history of strength and fatigue in dystrophin-, dystrophin/utrophin-, and laminin alpha2-deficient mice
    A M Connolly
    Department of Neurology, Washington University School of Medicine, Box 8111 660 S Euclid, Saint Louis, MO 63110, USA
    Neuromuscul Disord 11:703-12. 2001
    ..This work demonstrates a distinct pattern of disease progression in each model and provides a foundation for assessing strategies for improving strength in each model...
  12. doi request reprint Motor neuropathies and serum IgM binding to NS6S heparin disaccharide or GM1 ganglioside
    Alan Pestronk
    Department of Neurology, Washington University in St Louis School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA
    J Neurol Neurosurg Psychiatry 81:726-30. 2010
    ..This study compared the frequency and clinical associations of serum IgM binding to a different antigen, a disulphated heparin disaccharide (NS6S), with results of IgM binding to GM1...
  13. pmc The muscle protein dysferlin accumulates in the Alzheimer brain
    James E Galvin
    Alzheimer Disease Research Center, Washington University School of Medicine, 4488 Forest Park, Suite 130, St Louis, MO 63108, USA
    Acta Neuropathol 112:665-71. 2006
    ..In muscle, dysferlin plays a role in the repair of muscle membrane damage. The accumulation of dysferlin in the AD brain may be related to the inability of neurons to repair damage due to A beta deposits accumulating in the AD brain...
  14. ncbi request reprint Altered axonal mitochondrial transport in the pathogenesis of Charcot-Marie-Tooth disease from mitofusin 2 mutations
    Robert H Baloh
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Neurosci 27:422-30. 2007
    ....
  15. ncbi request reprint Transgenic expression of inclusion body myopathy associated mutant p97/VCP causes weakness and ubiquitinated protein inclusions in mice
    Conrad C Weihl
    Department of Neurology, Washington University School of Medicine, 660 S Euclid Avenue, Saint Louis, MO 63110, USA
    Hum Mol Genet 16:919-28. 2007
    ..TgVCP-RH animals will be a valuable tool for understanding the pathogenesis of IBM and the role of the UPS in skeletal muscle...
  16. doi request reprint Calibrated quantitative ultrasound imaging of skeletal muscle using backscatter analysis
    Craig M Zaidman
    Department of Neurology, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA
    Muscle Nerve 38:893-8. 2008
    ..Calibrated measurements of muscle backscatter have sensitivity and specificity in identifying and reliably measuring levels of skeletal muscle pathology...
  17. pmc Valosin-containing protein disease: inclusion body myopathy with Paget's disease of the bone and fronto-temporal dementia
    Conrad C Weihl
    Department of Neurology, Washington University School of Medicine, Saint Louis, MO 63110, USA
    Neuromuscul Disord 19:308-15. 2009
    ....
  18. doi request reprint Peripheral nerve size in normals and patients with polyneuropathy: an ultrasound study
    Craig M Zaidman
    Washington University School of Medicine, Department of Neurology, 660 S Euclid Avenue, Box 8111, St Louis, Missouri 63110, USA
    Muscle Nerve 40:960-6. 2009
    ..We conclude that NCSA measured by ultrasound is a quantifiable marker of nerve features that should be corrected for patient characteristics and nerve site. NCSA is generally larger in demyelinating than it is in axonal polyneuropathies...
  19. pmc Myosin binding protein C1: a novel gene for autosomal dominant distal arthrogryposis type 1
    Christina A Gurnett
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Hum Mol Genet 19:1165-73. 2010
    ..These findings reveal that the MYBPC1 is a novel gene responsible for DA1, though the mechanism of disease may differ from how some cardiac MYBPC3 mutations cause hypertrophic cardiomyopathy...
  20. doi request reprint Vascular pathology in dermatomyositis and anatomic relations to myopathology
    Alan Pestronk
    Department of Neurology, Washington University School of Medicine, 660 South Euclid Avenue, Box 8111, St Louis, Missouri 63110, USA
    Muscle Nerve 42:53-61. 2010
    ..Chronic immune vascular damage and insufficiency in dermatomyositis may cause ischemia, myofiber atrophy, and capillary damage in "watershed" regions of muscle near the avascular perimysium...
  21. pmc Sporadic inclusion body myositis: possible pathogenesis inferred from biomarkers
    Conrad C Weihl
    Department of Neurology and Hope Center for Neurological Disorders, Washington University School of Medicine, 660 S Euclid Avenue, Saint Louis, Missouri 63110, USA
    Curr Opin Neurol 23:482-8. 2010
    ..Our review will discuss current studies on these protein biomarkers and their utility in sIBM diagnosis...
  22. pmc Quantitative ultrasound using backscatter analysis in Duchenne and Becker muscular dystrophy
    Craig M Zaidman
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Neuromuscul Disord 20:805-9. 2010
    ..Longitudinal studies are required to determine the sensitivity of this measure to changes in pathology over time...
  23. pmc Novel GNE mutations in two phenotypically distinct HIBM2 patients
    Conrad C Weihl
    Department of Neurology and Hope Center for Neurological Disorders, Washington University School of Medicine, 660 S Euclid Avenue, Saint Louis, MO 63110, USA
    Neuromuscul Disord 21:102-5. 2011
    ..His muscle biopsy showed prominent necrosis without rimmed vacuoles. This study expands the phenotype and illustrates the clinical spectrum of HIBM2 identified in a U.S. based neuromuscular clinic...
  24. ncbi request reprint Inflammatory demyelinating neuropathies
    Glenn Lopate
    Department of Neurology, Washington University School of Medicine, 660 South Euclid Avenue, Campus Box 8111, St Louis, MO, 63110, USA
    Curr Treat Options Neurol 13:131-42. 2011
    ..Patients who do not respond to initial therapy, experience adverse effects from the initial immunomodulating agent, or require chronic treatment can be treated with another first-line agent or one of several second-line agents...
  25. ncbi request reprint Familial parkinsonism and ophthalmoplegia from a mutation in the mitochondrial DNA helicase twinkle
    Robert H Baloh
    Department of Neurology, Washington University School of Medicine, PO Box 8111, 660 S Euclid Ave, St Louis, MO 63110, USA
    Arch Neurol 64:998-1000. 2007
    ..To describe the clinical phenotype and genetic basis of a family with autosomal dominant progressive external ophthalmoplegia and parkinsonism from a Twinkle mutation...
  26. ncbi request reprint Inclusion body myopathy-associated mutations in p97/VCP impair endoplasmic reticulum-associated degradation
    Conrad C Weihl
    Department of Neurology, Washington University School of Medicine, 660 South Euclid Avenue, St Louis, MO 63110, USA
    Hum Mol Genet 15:189-99. 2006
    ..Undegraded mutant DeltaF508-CFTR also accumulates in these aggregates. We conclude that IBMPFD mutations in p97/VCP disrupt ERAD and that this may contribute to the pathogenesis of IBMPFD...
  27. ncbi request reprint Brachio-cervical inflammatory myopathies: clinical, immune, and myopathologic features
    Alan Pestronk
    Washington University School of Medicine, Department of Neurology, St Louis, Missouri 63110, USA
    Arthritis Rheum 54:1687-96. 2006
    ..To characterize patients with inflammatory myopathies who present with weakness in the proximal regions of the arms...
  28. ncbi request reprint Severe sensory ataxia and demyelinating polyneuropathy with IgM anti-GM2 and GalNAc-GD1A antibodies
    Glenn Lopate
    Department of Neurology, Box 8111, Washington University School of Medicine, 660 South Euclid Ave, St Louis, Missouri 63110, USA
    Muscle Nerve 25:828-36. 2002
    ..Diagnosis of this syndrome is important to direct appropriate treatment...
  29. ncbi request reprint Complement 3 deficiency and oral prednisolone improve strength and prolong survival of laminin alpha2-deficient mice
    Anne M Connolly
    Department of Neurology, Washington University School of Medicine, 660 S Euclid Ave, St Louis, MO 63110, USA
    J Neuroimmunol 127:80-7. 2002
    ..Because complement activity may be modified pharmacologically, this work may have implications for treatment of children with congenital muscular dystrophy secondary to laminin alpha2 deficiency...
  30. ncbi request reprint Peripheral neuropathy in an outpatient cohort of patients with Sjögren's syndrome
    Glenn Lopate
    Department of Neurology Washington University School of Medicine, 660 South Euclid Avenue, St Louis, Missouri 63110, USA
    Muscle Nerve 33:672-6. 2006
    ..Large-fiber dysfunction (as measured by testing vibration, deep tendon reflexes, and NCSs) was similar between the two groups. We conclude that small-fiber neuropathy is common in patients with SS...
  31. ncbi request reprint Treatment of chronic inflammatory demyelinating polyneuropathy with high-dose intermittent intravenous methylprednisolone
    Glenn Lopate
    Washington University School of Medicine, Department of Neurology, St Louis, MO 63110, USA
    Arch Neurol 62:249-54. 2005
    ..However, there is no consensus on initial therapy, and both of these treatments have drawbacks with long-term treatment...
  32. pmc Mutations in the tail domain of DYNC1H1 cause dominant spinal muscular atrophy
    M B Harms
    Department of Neurology, Hope Center for Neurological Disease, Washington University School of Medicine, St Louis, MO, USA
    Neurology 78:1714-20. 2012
    ..To identify the gene responsible for 14q32-linked dominant spinal muscular atrophy with lower extremity predominance (SMA-LED, OMIM 158600)...
  33. ncbi request reprint Organ-specific autoantibodies with muscle weakness
    M Al-Lozi
    Washington University in Saint Louis, Department of Neurology, Missouri 63110, USA
    Curr Opin Rheumatol 11:483-8. 1999
    ....
  34. pmc Dominant spinal muscular atrophy with lower extremity predominance: linkage to 14q32
    M B Harms
    Department of Neurology, Washington University School of Medicine, St Louis, MO 63110, USA
    Neurology 75:539-46. 2010
    ..We aimed to clinically, pathologically, and genetically characterize a large North American family with an autosomal dominant proximal SMA...
  35. ncbi request reprint Frequent atrophic groups with mixed-type myofibers is distinctive to motor neuron syndromes
    Robert H Baloh
    Department of Neurology, Washington University in St Louis, Box 8111, 660 South Euclid Avenue, St Louis, Missouri, USA
    Muscle Nerve 36:107-10. 2007
    ..The muscle biopsy pattern of frequent atrophic groups containing mixed fiber types should suggest a diagnosis of a motor neuron syndrome or motor neuropathy...
  36. ncbi request reprint An unusual pathologic feature associated with dermatomyositis
    Jacinda B Sampson
    Department of Neurology, University of Utah, Salt Lake City, UT, USA
    Neuromuscul Disord 16:391-3. 2006
    ....
  37. pmc TDP-43 accumulation in inclusion body myopathy muscle suggests a common pathogenic mechanism with frontotemporal dementia
    C C Weihl
    Department of Neurology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    J Neurol Neurosurg Psychiatry 79:1186-9. 2008
    ..This study adds sIBM and hereditary inclusion body myopathies to the growing list of TDP-43 positive inclusion diseases...
  38. ncbi request reprint A randomized efficacy and safety trial of oxandrolone in the treatment of Duchenne dystrophy
    G M Fenichel
    Department of Neurology, Ohio State University College of Medicine, USA
    Neurology 56:1075-9. 2001
    ..A pilot study suggested that oxandrolone, an anabolic steroid, improved strength in boys with Duchenne dystrophy (DD) and indicated the need for a more definitive study...
  39. ncbi request reprint Paraneoplastic myopathy: response to intravenous immunoglobulin
    J B Sampson
    Department of Neurology, University of Utah, Salt Lake City, UT, USA
    Neuromuscul Disord 17:404-8. 2007
    ..These cases highlight the role of histopathologic diagnosis in directing the treatment of paraneoplastic myopathy, and the role for IVIG in treatment of the syndrome...
  40. ncbi request reprint Frequency of spinal arteriovenous malformations in patients with unexplained myelopathy
    R G Strom
    ntional Neuroradiology Service, Mallinckrodt Institute of Radiology, Washington University School of Medicine, St Louis, MO, USA
    Neurology 66:928-31. 2006
    ..Spinal angiography should be performed in all patients with unexplained myelopathy after neurologic evaluation and an MRI demonstrating increased T2 signal or flow voids...
  41. ncbi request reprint Primary myopathy and accumulation of PrPSc-like molecules in peripheral tissues of transgenic mice expressing a prion protein insertional mutation
    R Chiesa
    Department of Cell Biology and Physiology, Washington University School of Medicine, St Louis, Missouri 63110, USA
    Neurobiol Dis 8:279-88. 2001
    ....
  42. doi request reprint A phase I/IItrial of MYO-029 in adult subjects with muscular dystrophy
    Kathryn R Wagner
    Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD 21287 7519, USA
    Ann Neurol 63:561-71. 2008
    ..We conducted a safety trial of a neutralizing antibody to myostatin, MYO-029, in adult muscular dystrophies (Becker muscular dystrophy, facioscapulohumeral dystrophy, and limb-girdle muscular dystrophy)...
  43. ncbi request reprint Treatment recommendations in Waldenstrom's macroglobulinemia: consensus panel recommendations from the Second International Workshop on Waldenstrom's Macroglobulinemia
    Morie A Gertz
    Mayo Clinic, Rochester, MN, USA
    Semin Oncol 30:121-6. 2003
    ..11) Corticosteroids may be useful in the treatment of symptomatic mixed cryoglobulinemia. (12) Splenectomy is rarely indicated but has been used to manage painful splenomegaly and hypersplenism...
  44. ncbi request reprint Human monoclonal macroglobulins with antibody activity
    Marvin J Stone
    Baylor Charles A Sammons Cancer Center, Dallas, TX 75246, USA
    Semin Oncol 30:318-24. 2003
    ..quot; Characterization of antigen-binding activities may provide insight into the pathogenesis of monoclonal gammopathies...
  45. ncbi request reprint Antibody-associated polyneuropathy syndromes: principles and treatment
    Andrew J Kornberg
    Department of Neurology, Royal Children s Hospital, Parkville, Victoria, Australia
    Semin Neurol 23:181-90. 2003
    ..The general principles regarding therapy of immune neuropathies will be discussed with a focus on diagnosis and treatment options of the demyelinating and immunoglobulin M antibody-associated neuropathies...
  46. ncbi request reprint Inclusion body myopathy associated with Paget disease of bone and frontotemporal dementia is caused by mutant valosin-containing protein
    Giles D J Watts
    Division of Genetics, Children s Hospital Boston, 300 Longwood Avenue, Harvard Medical School, Boston, Massachusetts 02115, USA
    Nat Genet 36:377-81. 2004
    ..Identification of VCP as causing IBMPFD has important implications for other inclusion-body diseases, including myopathies, dementias and Paget disease of bone (PDB), as it may define a new common pathological ubiquitin-based pathway...
  47. ncbi request reprint Novel ubiquitin neuropathology in frontotemporal dementia with valosin-containing protein gene mutations
    Mark S Forman
    Department of Pathology, University of Pennsylvania School of Medicine, Philadelphia, 19104, USA
    J Neuropathol Exp Neurol 65:571-81. 2006
    ..Our findings are consistent with the hypothesis that the pathology associated with VCP gene mutations is the result of impairment of ubiquitin-based degradation pathways...
  48. pmc Amyotrophic lateral sclerosis: an emerging era of collaborative gene discovery
    Katrina Gwinn
    National Institute for Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States of America
    PLoS ONE 2:e1254. 2007
    ..This resource should facilitate genetic discoveries which we anticipate will ultimately provide a better understanding of the biological mechanisms of neurodegeneration in ALS...
  49. ncbi request reprint Limb-girdle muscular dystrophy in the United States
    Steven A Moore
    University of Iowa, Iowa City, 52242, USA
    J Neuropathol Exp Neurol 65:995-1003. 2006
    ..The most common LGMDs in the United States are calpainopathies, dysferlinopathies, sarcoglycanopathies, and dystroglycanopathies...
  50. doi request reprint Update of the Pompe disease mutation database with 107 sequence variants and a format for severity rating
    Marian Kroos
    Departments of Clinical Genetics and Pediatrics, Erasmus MC, Rotterdam, The Netherlands
    Hum Mutat 29:E13-26. 2008
    ..Further, this article introduces a tool to rate the various mutations by severity, which will improve understanding of the genotype-phenotype correlation and facilitate the diagnosis and prognosis in Pompe disease...
  51. ncbi request reprint Whole-genome analysis of sporadic amyotrophic lateral sclerosis
    Travis Dunckley
    Translational Genomics Research Inst, Phoenix, AZ 85004, USA
    N Engl J Med 357:775-88. 2007
    ..Approximately 90% of persons with amyotrophic lateral sclerosis (ALS) have the sporadic form, which may be caused by the interaction of multiple environmental factors and previously unknown genes...
  52. ncbi request reprint CINRG randomized controlled trial of creatine and glutamine in Duchenne muscular dystrophy
    Diana M Escolar
    Children s National Medical Center, George Washington University, Washington, DC, USA
    Ann Neurol 58:151-5. 2005
    ..Creatine and glutamine were well tolerated...