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
Two sodium channels contribute to the TTX-R sodium current in primary sensory neurons.
Authors: Authors: Tate S, Benn S, Hick C, Trezise D, John V, Mannion RJ, Costigan M, Plumpton C, Grose D, Gladwell Z, Kendall G, Dale K, Bountra C, Woolf CJ.
Nat Neurosci
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Towards a mechanism-based classification of pain?
Authors: Authors: Woolf CJ, Bennett GJ, Doherty M, Dubner R, Kidd B, Koltzenburg M, Lipton R, Loeser JD, Payne R, Torebjork E.
Pain
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Heat shock protein 27: developmental regulation and expression after peripheral nerve injury.
Authors: Authors: Costigan M, Mannion RJ, Kendall G, Lewis SE, Campagna JA, Coggeshall RE, Meridith-Middleton J, Tate S, Woolf CJ.
J Neurosci
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High efficiency gene transfer to the central nervous system of rodents and primates using herpes virus vectors lacking functional ICP27 and ICP34.5.
Authors: Authors: Howard MK, Kershaw T, Gibb B, Storey N, MacLean AR, Zeng BY, Tel BC, Jenner P, Brown SM, Woolf CJ, Anderson PN, Coffin RS, Latchman DS.
Gene Ther
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Leukemia inhibitory factor is an anti-inflammatory and analgesic cytokine.
Authors: Authors: Banner LR, Patterson PH, Allchorne A, Poole S, Woolf CJ.
J Neurosci
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Identification of somatostatin sst2(a) receptor expressing neurones in central regions involved in nociception.
Authors: Authors: Schindler M, Holloway S, Hathway G, Woolf CJ, Humphrey PP, Emson PC.
Brain Res
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Morphine, the NMDA receptor antagonist MK801 and the tachykinin NK1 receptor antagonist RP67580 attenuate the development of inflammation-induced progressive tactile hypersensitivity.
Authors: Authors: Ma QP, Allchorne AJ, Woolf CJ.
Pain
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Null mutations lacking substance: elucidating pain mechanisms by genetic pharmacology.
Authors: Authors: Woolf CJ, Mannion RJ, Neumann S.
Neuron
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Deafferentation is insufficient to induce sprouting of A-fibre central terminals in the rat dorsal horn.
Authors: Authors: Mannion RJ, Doubell TP, Gill H, Woolf CJ.
J Comp Neurol
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Growth-associated protein 43 immunoreactivity in the superficial dorsal horn of the rat spinal cord is localized in atrophic C-fiber, and not in sprouted A-fiber, central terminals after peripheral nerve injury.
Authors: Authors: Doubell TP, Woolf CJ.
J Comp Neurol
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