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
Central sensitization: a generator of pain hypersensitivity by central neural plasticity.
Authors: Authors: Latremoliere A, Woolf CJ.
J Pain
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Coapplication of lidocaine and the permanently charged sodium channel blocker QX-314 produces a long-lasting nociceptive blockade in rodents.
Authors: Authors: Binshtok AM, Gerner P, Oh SB, Puopolo M, Suzuki S, Roberson DP, Herbert T, Wang CF, Kim D, Chung G, Mitani AA, Wang GK, Bean BP, Woolf CJ.
Anesthesiology
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Mu and delta opioid receptors diverge.
Authors: Authors: Woolf CJ.
Cell
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A novel tool for the assessment of pain: validation in low back pain.
Authors: Authors: Scholz J, Mannion RJ, Hord DE, Griffin RS, Rawal B, Zheng H, Scoffings D, Phillips A, Guo J, Laing RJ, Abdi S, Decosterd I, Woolf CJ.
PLoS Med
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Periganglionic inflammation elicits a distally radiating pain hypersensitivity by promoting COX-2 induction in the dorsal root ganglion.
Authors: Authors: Amaya F, Samad TA, Barrett L, Broom DC, Woolf CJ.
Pain
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COX2 in CNS neural cells mediates mechanical inflammatory pain hypersensitivity in mice.
Authors: Authors: Vardeh D, Wang D, Costigan M, Lazarus M, Saper CB, Woolf CJ, Fitzgerald GA, Samad TA.
J Clin Invest
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Transient receptor potential channels: targeting pain at the source.
Authors: Authors: Patapoutian A, Tate S, Woolf CJ.
Nat Rev Drug Discov
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Neuropathic pain: a maladaptive response of the nervous system to damage.
Authors: Authors: Costigan M, Scholz J, Woolf CJ.
Annu Rev Neurosci
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Nociceptors are interleukin-1beta sensors.
Authors: Authors: Binshtok AM, Wang H, Zimmermann K, Amaya F, Vardeh D, Shi L, Brenner GJ, Ji RR, Bean BP, Woolf CJ, Samad TA.
J Neurosci
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Capsaicin combined with local anesthetics preferentially prolongs sensory/nociceptive block in rat sciatic nerve.
Authors: Authors: Gerner P, Binshtok AM, Wang CF, Hevelone ND, Bean BP, Woolf CJ, Wang GK.
Anesthesiology
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