Joachim Scholz

Summary

Affiliation: Harvard University
Country: USA

Publications

  1. ncbi Blocking caspase activity prevents transsynaptic neuronal apoptosis and the loss of inhibition in lamina II of the dorsal horn after peripheral nerve injury
    Joachim Scholz
    Department of Anesthesia and Critical Care, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neurosci 25:7317-23. 2005
  2. ncbi Endogenous tetrahydroisoquinolines associated with Parkinson's disease mimic the feedback inhibition of tyrosine hydroxylase by catecholamines
    Joachim Scholz
    Neurochemistry Research Group, Department of Neurology, University of Lubeck, Germany
    FEBS J 275:2109-21. 2008
  3. pmc A novel tool for the assessment of pain: validation in low back pain
    Joachim Scholz
    Department of Anesthesia and Critical Care, Massachusetts General Hospital, Boston, Massachusetts, United States of America
    PLoS Med 6:e1000047. 2009
  4. ncbi The neuropathic pain triad: neurons, immune cells and glia
    Joachim Scholz
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA
    Nat Neurosci 10:1361-8. 2007
  5. pmc Increased systemic levels of norsalsolinol derivatives are induced by levodopa treatment and do not represent biological markers of Parkinson's disease
    J Scholz
    Neurochemistry Research Group, Department of Neurology, Medical University of Lubeck, Lubeck, Germany
    J Neurol Neurosurg Psychiatry 75:634-6. 2004
  6. pmc Low-dose methotrexate reduces peripheral nerve injury-evoked spinal microglial activation and neuropathic pain behavior in rats
    Joachim Scholz
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, 149 13th Street, Room 4309, Charlestown, MA 02129, USA
    Pain 138:130-42. 2008
  7. pmc Neuropathic pain: a maladaptive response of the nervous system to damage
    Michael Costigan
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02129, USA
    Annu Rev Neurosci 32:1-32. 2009
  8. ncbi Partial peripheral nerve injury promotes a selective loss of GABAergic inhibition in the superficial dorsal horn of the spinal cord
    Kimberly A Moore
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neurosci 22:6724-31. 2002
  9. ncbi Complement induction in spinal cord microglia results in anaphylatoxin C5a-mediated pain hypersensitivity
    Robert S Griffin
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neurosci 27:8699-708. 2007
  10. ncbi GTP cyclohydrolase and tetrahydrobiopterin regulate pain sensitivity and persistence
    Irmgard Tegeder
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, 149 13th Street, Room 4309, Charlestown, Massachusetts 02129, USA
    Nat Med 12:1269-77. 2006

Research Grants

Detail Information

Publications19

  1. ncbi Blocking caspase activity prevents transsynaptic neuronal apoptosis and the loss of inhibition in lamina II of the dorsal horn after peripheral nerve injury
    Joachim Scholz
    Department of Anesthesia and Critical Care, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neurosci 25:7317-23. 2005
    ..Preventing nerve injury-induced apoptosis of dorsal horn neurons by blocking caspase activity maintains inhibitory transmission in lamina II and reduces pain hypersensitivity...
  2. ncbi Endogenous tetrahydroisoquinolines associated with Parkinson's disease mimic the feedback inhibition of tyrosine hydroxylase by catecholamines
    Joachim Scholz
    Neurochemistry Research Group, Department of Neurology, University of Lubeck, Germany
    FEBS J 275:2109-21. 2008
    ..Increased levels of N-methyl-norsalsolinol and related tetrahydroisoquinolines are therefore likely to accelerate dopamine depletion in Parkinson's disease...
  3. pmc A novel tool for the assessment of pain: validation in low back pain
    Joachim Scholz
    Department of Anesthesia and Critical Care, Massachusetts General Hospital, Boston, Massachusetts, United States of America
    PLoS Med 6:e1000047. 2009
    ..We have developed a tool for a standardized assessment of pain-related symptoms and signs that differentiates pain phenotypes independent of etiology...
  4. ncbi The neuropathic pain triad: neurons, immune cells and glia
    Joachim Scholz
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA
    Nat Neurosci 10:1361-8. 2007
    ....
  5. pmc Increased systemic levels of norsalsolinol derivatives are induced by levodopa treatment and do not represent biological markers of Parkinson's disease
    J Scholz
    Neurochemistry Research Group, Department of Neurology, Medical University of Lubeck, Lubeck, Germany
    J Neurol Neurosurg Psychiatry 75:634-6. 2004
    ....
  6. pmc Low-dose methotrexate reduces peripheral nerve injury-evoked spinal microglial activation and neuropathic pain behavior in rats
    Joachim Scholz
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, 149 13th Street, Room 4309, Charlestown, MA 02129, USA
    Pain 138:130-42. 2008
    ..We confirm that microglial activation is crucial for the development of pain after nerve injury, and demonstrates that suppression of this cellular immune response is a promising approach for preventing neuropathic pain...
  7. pmc Neuropathic pain: a maladaptive response of the nervous system to damage
    Michael Costigan
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02129, USA
    Annu Rev Neurosci 32:1-32. 2009
    ..Treatment needs to move from merely suppressing symptoms to a disease-modifying strategy aimed at both preventing maladaptive plasticity and reducing intrinsic risk...
  8. ncbi Partial peripheral nerve injury promotes a selective loss of GABAergic inhibition in the superficial dorsal horn of the spinal cord
    Kimberly A Moore
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neurosci 22:6724-31. 2002
    ..Both of these mechanisms could reduce presynaptic GABA levels and promote a functional loss of GABAergic transmission in the superficial dorsal horn...
  9. ncbi Complement induction in spinal cord microglia results in anaphylatoxin C5a-mediated pain hypersensitivity
    Robert S Griffin
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA
    J Neurosci 27:8699-708. 2007
    ..We conclude that induction of the complement cascade in spinal cord microglia after peripheral nerve injury contributes to neuropathic pain through the release and action of the C5a anaphylatoxin peptide...
  10. ncbi GTP cyclohydrolase and tetrahydrobiopterin regulate pain sensitivity and persistence
    Irmgard Tegeder
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, 149 13th Street, Room 4309, Charlestown, Massachusetts 02129, USA
    Nat Med 12:1269-77. 2006
    ..BH4 is therefore an intrinsic regulator of pain sensitivity and chronicity, and the GTP cyclohydrolase haplotype is a marker for these traits...
  11. ncbi Hsp27 upregulation and phosphorylation is required for injured sensory and motor neuron survival
    Susanna C Benn
    Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Charlestown, MA 02129, USA
    Neuron 36:45-56. 2002
    ..Transcriptional and posttranslational regulation of Hsp27 is necessary for sensory and motor neuron survival following peripheral nerve injury...
  12. ncbi Modification of tyrosine hydroxylase activity by chloral derived beta-carbolines in vitro
    Franz Riederer
    Neurochemical Research Group, Department of Neurology, Medical University of Lubeck, Ratzeburger Allee 160, D 23538 Lubeck, Germany
    J Neurochem 81:814-9. 2002
    ..We suggest that these beta-carbolines modulate dopamine synthesis by interacting with a protein kinase TH-activating system...
  13. pmc Peripheral nerve injury produces a sustained shift in the balance between glutamate release and uptake in the dorsal horn of the spinal cord
    Perrine Inquimbert
    F M Kirby Neurobiology Center, Children s Hospital and Harvard Medical School, Boston, MA, USA
    Pain 153:2422-31. 2012
    ..Balancing glutamate release and uptake after nerve injury should be an important target in the management of chronic neuropathic pain...
  14. ncbi Can we conquer pain?
    Joachim Scholz
    Neural Plasticity Research Group, Department of Anesthesia, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02129, USA
    Nat Neurosci 5:1062-7. 2002
    ..Elucidation of these mechanisms is key to the development of treatments that specifically target underlying causes rather than just symptoms. This new approach promises to revolutionize pain diagnosis and management...
  15. ncbi Pituitary adenylate cyclase-activating polypeptide (PACAP-27) enhances tyrosine hydroxylase activity in the nucleus accumbens of the rat
    A Moser
    Neurochemical Research Group, Department of Neurology, Medical University of Lubeck, Lubeck, Germany
    Neuropeptides 33:492-7. 1999
    ..This report's data suggest that PACAP-27 activates TyrOH in the rat nucleus accumbens through receptor-mediated cAMP formation. The exact receptor type present in the nucleus accumbens has yet not been specified...
  16. ncbi N-methyl-norsalsolinol, an endogenous neurotoxin, inhibits tyrosine hydroxylase activity in the rat brain nucleus accumbens in vitro
    J Scholz
    Department of Neurology, Medical University of Lubeck, Germany
    Neurochem Int 31:845-9. 1997
    ..Since previous investigations have moreover demonstrated a cytotoxic potential of 2-MDTIQ, these findings require special attention. 2-MDTIQ may represent an essential factor in the degenerative process of Parkinson's disease...
  17. ncbi Modeled ligand-protein complexes elucidate the origin of substrate specificity and provide insight into catalytic mechanisms of phenylalanine hydroxylase and tyrosine hydroxylase
    Astrid Maass
    Fraunhofer Institute for Algorithms and Scientific Computing SCAI, Schloss Birlinghoven, Sankt Augustin, Germany
    Eur J Biochem 270:1065-75. 2003
    ..Electrostatic forces play a key role in hindering the bidentate binding of the immediate reaction product l-DOPA to TH, thereby saving the enzyme from direct feedback inhibition...
  18. ncbi 1-Trichloromethyl-1,2,3,4-tetrahydro-beta-carboline (TaClo) and related derivatives: chemistry and biochemical effects on catecholamine biosynthesis
    Gerhard Bringmann
    Institut fur Organische Chemie, Universitat Wurzburg, Am Hubland, D 97074 Wurzburg, Germany
    Bioorg Med Chem 10:2207-14. 2002
    ....
  19. ncbi Using screening tools to identify neuropathic pain
    Michael I Bennett
    Clinical Teaching and Research Unit, St Gemma s Hospice, 329 Harrogate Road, Leeds LS17 6QD, UK
    Pain 127:199-203. 2007

Research Grants1

  1. Transsynaptic Neurodegeneration after Nerve Injury
    Joachim Scholz; Fiscal Year: 2007
    ..We will determine if rescuing dorsal horn interneurons preserves spinal inhibition and attenuates neuropathic pain-like behavior. ..