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
Novel analgesic development: from target to patient or patient to target?
Authors: Authors: Woolf CJ.
Curr Opin Investig Drugs
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Bradykinin enhances AMPA and NMDA receptor activity in spinal cord dorsal horn neurons by activating multiple kinases to produce pain hypersensitivity.
Authors: Authors: Kohno T, Wang H, Amaya F, Brenner GJ, Cheng JK, Ji RR, Woolf CJ.
J Neurosci
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Ro5-4864 promotes neonatal motor neuron survival and nerve regeneration in adult rats.
Authors: Authors: Mills C, Makwana M, Wallace A, Benn S, Schmidt H, Tegeder I, Costigan M, Brown RH, Raivich G, Woolf CJ.
Eur J Neurosci
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The neuropathic pain triad: neurons, immune cells and glia.
Authors: Authors: Scholz J, Woolf CJ.
Nat Neurosci
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Inhibition of nociceptors by TRPV1-mediated entry of impermeant sodium channel blockers.
Authors: Authors: Binshtok AM, Bean BP, Woolf CJ.
Nature
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GDNF selectively promotes regeneration of injury-primed sensory neurons in the lesioned spinal cord.
Authors: Authors: Mills CD, Allchorne AJ, Griffin RS, Woolf CJ, Costigan M.
Mol Cell Neurosci
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Complement induction in spinal cord microglia results in anaphylatoxin C5a-mediated pain hypersensitivity.
Authors: Authors: Griffin RS, Costigan M, Brenner GJ, Ma CH, Scholz J, Moss A, Allchorne AJ, Stahl GL, Woolf CJ.
J Neurosci
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Nociceptors--noxious stimulus detectors.
Authors: Authors: Woolf CJ, Ma Q.
Neuron
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Delayed sympathetic dependence in the spared nerve injury (SNI) model of neuropathic pain.
Authors: Authors: Pertin M, Allchorne AJ, Beggah AT, Woolf CJ, Decosterd I.
Mol Pain
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ATF3 increases the intrinsic growth state of DRG neurons to enhance peripheral nerve regeneration.
Authors: Authors: Seijffers R, Mills CD, Woolf CJ.
J Neurosci
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