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
Neuroscience
Authors: Authors: The growth-associated protein GAP-43 appears in dorsal root ganglion cells and in the dorsal horn of the rat spinal cord following peripheral nerve injury
1990; 34(2):465-78.
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J Neurosci
Authors: Authors: Alterations in the structure, function, and chemistry of C fibers following local application of vinblastine to the sciatic nerve of the rat
1984 Feb; 4(2):430-41.
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Neuropharmacology
Authors: Authors: Pyrogen and prostaglandin fever in the rabbit-I: Effects of salicylate and the role of cyclic AMP
1975 May-Jun; 14(5-6):397-403.
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J Comp Neurol
Authors: Authors: Reorganization of central terminals of myelinated primary afferents in the rat dorsal horn following peripheral axotomy
1995 Sep 11; 360(1):121-34.
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Acta Neurochir Suppl (Wien)
Authors: Authors: The pathophysiology of peripheral neuropathic pain--abnormal peripheral input and abnormal central processing
1993; 58:125-30.
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Nature
Authors: Authors: Dynamic receptive field plasticity in rat spinal cord dorsal horn following C-primary afferent input
1987 Jan 8-14; 325(7000):151-3.
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Brain Res
Authors: Authors: Intrathecal high dose morphine produces hyperalgesia in the rat
1981 Mar 30; 209(2):491-5.
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Cell Rep
Authors: Authors: Sensory neurons display cell-type-specific vulnerability to loss of neuron-glia interactions
2022 Jul 19; 40(3):111130.
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Exp Neurol
Authors: Authors: The downregulation of GAP-43 is not responsible for the failure of regeneration in freeze-killed nerve grafts in the rat
1994 Oct; 129(2):311-20.
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Neuroscience
Authors: Authors: Time-dependent differences in the increase in GAP-43 expression in dorsal root ganglion cells after peripheral axotomy
1991; 45(1):213-20.
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