Clifford Woolf

Clifford Woolf, MB, BCh, PhD

Professor of Neurology, Harvard Medical School

Adaptive and Maladaptive Plasticity in Sensory and Motor Systems

Neurons are subject to functional, chemical and structural plasticity. This plasticity is an important factor both in the normal function of the nervous system and in a vast range of neurological diseases.

The Woolf lab studies how different forms of neuronal plasticity contribute both to adaptive and maladaptive changes in the mammalian nervous system, particularly in relation to pain, regeneration and neurodegenerative diseases.

Most of our work is concentrated on primary sensory and motor neurons, and to the interaction of neurons and immune cells, using a multidisciplinary approach spanning stem cell, molecular and cell biology, electrophysiology, neuroanatomy, behavior and genetics. We have established functional and comparative genomic strategies using expression profiling, bioinformatics and gain- and loss-of-function approaches, to screen for novel genes that contribute to neuronal plasticity and disease phenotypes. Our group works closely with many academic groups and the pharmaceutical industry to model disease and identify molecular targets for novel analgesics, axonal growth determinants and neuroprotective agents.

Current research includes study of the transcriptional control and post-translational processing of receptors and ion channels that mediate pain hypersensitivity, selective silencing of defined neuronal populations, intracellular signal transduction cascades activated by peripheral inflammation and nerve injury, neuro-immune interactions, transcription factors as master regulators of pain, growth and survival programs, cell survival in injured sensory and motor neurons, and the contribution of intrinsic growth determinants in establishing regenerative capacity in the peripheral and central nervous system. We are an active part of the Harvard Stem Cell Institute and are investigating how sensory and motor neurons reprogrammed from patient fibroblasts can be used to study pain and motor neuron disease and to screen for new treatments.

Publications View
Windup and central sensitization are not equivalent.
Authors: Authors: Woolf CJ.
Pain
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Expression of a developmentally regulated, phosphorylated isoform of microtubule-associated protein 1B in regenerating axons of the sciatic nerve.
Authors: Authors: Bush MS, Tonge DA, Woolf C, Gordon-Weeks PR.
Neuroscience
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Intrinsic versus extrinsic factors in determining the regeneration of the central processes of rat dorsal root ganglion neurons: the influence of a peripheral nerve graft.
Authors: Authors: Chong MS, Woolf CJ, Turmaine M, Emson PC, Anderson PN.
J Comp Neurol
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Zinc reduces the hyperalgesia and upregulation of NGF and IL-1 beta produced by peripheral inflammation in the rat.
Authors: Authors: Safieh-Garabedian B, Poole S, Allchorne A, Kanaan S, Saade N, Woolf CJ.
Neuropharmacology
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Peripheral cell types contributing to the hyperalgesic action of nerve growth factor in inflammation.
Authors: Authors: Woolf CJ, Ma QP, Allchorne A, Poole S.
J Neurosci
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Phenotypic modification of primary sensory neurons: the role of nerve growth factor in the production of persistent pain.
Authors: Authors: Woolf CJ.
Philos Trans R Soc Lond B Biol Sci
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Induction of the Oct-2 transcription factor in primary sensory neurons during inflammation is nerve growth factor-dependent.
Authors: Authors: Ensor E, Kendall G, Allchorne A, Woolf CJ, Latchman DS.
Neurosci Lett
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Influence of inflammation or disconnection from peripheral target tissue on the capsaicin sensitivity of rat dorsal root ganglion sensory neurones.
Authors: Authors: Hu-Tsai M, Woolf C, Winter J.
Neurosci Lett
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Overcoming inhibition
Authors: Authors: Spinal injury
Nature
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Prevention or elimination of central sensitization
Authors: Authors: A new strategy for the treatment of inflammatory pain
Drugs
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