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
Nociceptive-specific activation of ERK in spinal neurons contributes to pain hypersensitivity.
Authors: Authors: Ji RR, Baba H, Brenner GJ, Woolf CJ.
Nat Neurosci
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Semaphorin 3A growth cone collapse requires a sequence homologous to tarantula hanatoxin.
Authors: Authors: Behar O, Mizuno K, Badminton M, Woolf CJ.
Proc Natl Acad Sci U S A
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A role for HSP27 in sensory neuron survival.
Authors: Authors: Lewis SE, Mannion RJ, White FA, Coggeshall RE, Beggs S, Costigan M, Martin JL, Dillmann WH, Woolf CJ.
J Neurosci
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Neurotrophins: peripherally and centrally acting modulators of tactile stimulus-induced inflammatory pain hypersensitivity.
Authors: Authors: Mannion RJ, Costigan M, Decosterd I, Amaya F, Ma QP, Holstege JC, Ji RR, Acheson A, Lindsay RM, Wilkinson GA, Woolf CJ.
Proc Natl Acad Sci U S A
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Implications of recent advances in the understanding of pain pathophysiology for the assessment of pain in patients.
Authors: Authors: Woolf CJ, Decosterd I.
Pain
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Axonal regeneration from injured dorsal roots into the spinal cord of adult rats.
Authors: Authors: Chong MS, Woolf CJ, Haque NS, Anderson PN.
J Comp Neurol
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Transcriptional and posttranslational plasticity and the generation of inflammatory pain.
Authors: Authors: Woolf CJ, Costigan M.
Proc Natl Acad Sci U S A
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Pain.
Authors: Authors: Basbaum AI, Woolf CJ.
Curr Biol
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Neuropathic pain: aetiology, symptoms, mechanisms, and management.
Authors: Authors: Woolf CJ, Mannion RJ.
Lancet
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Regeneration of dorsal column fibers into and beyond the lesion site following adult spinal cord injury.
Authors: Authors: Neumann S, Woolf CJ.
Neuron
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