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
Identification and characterization of a novel human vanilloid receptor-like protein, VRL-2.
Authors: Authors: Delany NS, Hurle M, Facer P, Alnadaf T, Plumpton C, Kinghorn I, See CG, Costigan M, Anand P, Woolf CJ, Crowther D, Sanseau P, Tate SN.
Physiol Genomics
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Turbocharging neurons for growth: accelerating regeneration in the adult CNS.
Authors: Authors: Woolf CJ.
Nat Neurosci
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Changes in tactile stimuli-induced behavior and c-Fos expression in the superficial dorsal horn and in parabrachial nuclei after sciatic nerve crush.
Authors: Authors: Bester H, Beggs S, Woolf CJ.
J Comp Neurol
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Pain.
Authors: Authors: Woolf CJ.
Neurobiol Dis
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Contribution of central sensitisation to the development of non-cardiac chest pain.
Authors: Authors: Sarkar S, Aziz Q, Woolf CJ, Hobson AR, Thompson DG.
Lancet
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Pain: molecular mechanisms.
Authors: Authors: Costigan M, Woolf CJ.
J Pain
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Pain mechanisms and management: a central perspective.
Authors: Authors: Mannion RJ, Woolf CJ.
Clin J Pain
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Spared nerve injury: an animal model of persistent peripheral neuropathic pain.
Authors: Authors: Decosterd I, Woolf CJ.
Pain
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Resection of sciatic nerve re-triggers central sprouting of A-fibre primary afferents in the rat.
Authors: Authors: Ma QP, Tian L, Woolf CJ.
Neurosci Lett
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Delayed loss of small dorsal root ganglion cells after transection of the rat sciatic nerve.
Authors: Authors: Tandrup T, Woolf CJ, Coggeshall RE.
J Comp Neurol
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