Philadelphia University + Thomas Jefferson University

Elliott, Melanie B.

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Melanie B. Elliott, PhD

Melanie B. Elliott, PhD

Contact Dr. Elliott

1025 Walnut Street
Philadelphia, PA 19107

(215) 955-3776

Expertise & Research Interests

Our laboratory investigates secondary injury mechanisms implicated in the behavioral consequences of traumatic brain injury. Our research utilizes a variety of techniques to examine the cellular and molecular responses to injury in combination with pharmacologic or genetic modification of these responses. Our research investigates neuroimmune modulation as a neuroprotective strategy in a model of traumatic brain injury. We are particularly interested in the involvement of an endogenous neurotransmitter system, the endocannabinoid system, with a known role in both pathological and homeostatic functions in the injured CNS. In addition, projects in our laboratory investigate mechanisms underlying sensitization of the trigeminovascular system after traumatic brain injury with implications in the treatment of acute and chronic post-traumatic headache. Research support: Merck Inc.; Department of Defense


Most Recent Peer-Reviewed Publications

  1. Region-specific disruption of the blood-brain barrier following repeated inflammatory dural stimulation in a rat model of chronic trigeminal allodynia
  2. Frequent mild head injury promotes trigeminal sensitivity concomitant with microglial proliferation, astrocytosis, and increased neuropeptide levels in the trigeminal pain system
  3. Effectiveness of conservative interventions for sickness and pain behaviors induced by a high repetition high force upper extremity task
  4. The role of adenosine signaling in headache: A review
  5. 189 Comparison of Efficacy of Tonic and Burst Occipital Nerve Stimulation in Treating Trigeminal Allodynia: Chronic Result
  6. Trigeminal Pain Molecules, Allodynia, and Photosensitivity Are Pharmacologically and Genetically Modulated in a Model of Traumatic Brain Injury
  7. Sickness behaviors (reduced social interaction and pain behaviors) are linked to inflammatory mechanisms in a rat model of work-related musculoskeletal disorders
  8. IV and IP administration of rhodamine in visualization of WBC-BBB interactions in cerebral vessels
  9. Mechanical alloydnia induced by traumatic brain injury is independent of restraint stress
  10. Delayed thalamic astrocytosis and disrupted sleep-wake patterns in a preclinical model of traumatic brain injury
  11. Cannabinoid receptor type-2 stimulation, blockade, and deletion alter the vascular inflammatory responses to traumatic brain injury
  12. A cannabinoid type 2 receptor agonist attenuates blood-brain barrier damage and neurodegeneration in a murine model of traumatic brain injury
  13. Nociceptive neuropeptide increases and periorbital allodynia in a model of traumatic brain injury
  14. Acute effects of a selective cannabinoid-2 receptor agonist on neuroinflammation in a model of traumatic brain injury
  15. A murine model of hypertonic saline as a treatment for acute spinal cord injury: Effects on autonomic outcome - Laboratory investigation
  16. Performance of a repetitive task by aged rats leads to median neuropathy and spinal cord inflammation with associated sensorimotor declines
  17. Hypertonic saline attenuates tissue loss and astrocyte hypertrophy in a model of traumatic brain injury
  18. Spinal substance P and neurokinin-1 increase with high repetition reaching
  19. High force reaching task induces widespread inflammation, increased spinal cord neurochemicals and neuropathic pain
  20. Serum and tissue cytokines and chemokines increase with repetitive upper extremity tasks