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
Patrick D. Wall (1925-2001).
Authors: Authors: Woolf CJ.
Nature
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Developmental expression of the TTX-resistant voltage-gated sodium channels Nav1.8 (SNS) and Nav1.9 (SNS2) in primary sensory neurons.
Authors: Authors: Benn SC, Costigan M, Tate S, Fitzgerald M, Woolf CJ.
J Neurosci
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The paired homeodomain protein DRG11 is required for the projection of cutaneous sensory afferent fibers to the dorsal spinal cord.
Authors: Authors: Chen ZF, Rebelo S, White F, Malmberg AB, Baba H, Lima D, Woolf CJ, Basbaum AI, Anderson DJ.
Neuron
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A-fiber sensory input induces neuronal cell death in the dorsal horn of the adult rat spinal cord.
Authors: Authors: Coggeshall RE, Lekan HA, White FA, Woolf CJ.
J Comp Neurol
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Mechanism-based pain diagnosis: issues for analgesic drug development.
Authors: Authors: Woolf CJ, Max MB.
Anesthesiology
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Transport and localization of the DEG/ENaC ion channel BNaC1alpha to peripheral mechanosensory terminals of dorsal root ganglia neurons.
Authors: Authors: García-Añoveros J, Samad TA, Zuvela-Jelaska L, Woolf CJ, Corey DP.
J Neurosci
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Interleukin-1beta-mediated induction of Cox-2 in the CNS contributes to inflammatory pain hypersensitivity.
Authors: Authors: Samad TA, Moore KA, Sapirstein A, Billet S, Allchorne A, Poole S, Bonventre JV, Woolf CJ.
Nature
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Direct activation of rat spinal dorsal horn neurons by prostaglandin E2.
Authors: Authors: Baba H, Kohno T, Moore KA, Woolf CJ.
J Neurosci
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Differential gene expression--how to find new analgesic targets.
Authors: Authors: Befort K, Costigan M, Woolf CJ.
Curr Opin Investig Drugs
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Neuronal plasticity and signal transduction in nociceptive neurons: implications for the initiation and maintenance of pathological pain.
Authors: Authors: Ji RR, Woolf CJ.
Neurobiol Dis
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