Allison Harmel

Mentor: Dr. Colin Sumners
College of Medicine
"I chose to become involved in research so I could have the opportunity to have a more hands on experience with science. The science labs at the University of Florida are phenomenal however having your own research study really gives you the chance to become more independent and look into what really intrigues you. My research has given me the opportunity to investigate questions I would have never thought were possible."





Research Interests

  • Stroke
  • Renin-Angiotensin System
  • Inflammatory Response

Academic Awards

  • Deans List Fall 2013
  • Presidents Honor Roll Spring 2015
  • Deans List Spring 2016
  • University Scholars Program 2016


  • Panhellenic Director
  • Camp Kesem
  • Zeta Tau Alpha


  • Pediatric Cardiology Unit Volunteer

Hobbies and Interests

  • Running

Research Description

Inflammation in the Brain Post-Stroke: A Growing Problem

"Ischemic stroke is not only the most common stroke subtype but is one of the leading causes of death and disability in the United States. There are both acute and sustained inflammatory processes that occurs after stroke. This process involves the rapid activation of resident inflammatory cells (primarily microglia), activation of supporting astrocytes, and subsequent invasion of various types of inflammatory cells, including macrophages and T-cells. The result of this inflammatory activation eventually leads to disruption of the blood-brain barrier, brain edema, neuronal death, and hemorrhagic transformation. There have been recent findings that activation the protective axis of the renin angiotensin system (RAS) by agonists of angiotensin II type 2 receptors (AT2Rs) result in vasodilation and anti-inflammatory effects in peripheral tissues. Systemic administration of the drug compound-21 (C21), an agonist of AT2Rs, after stroke has also elicited profound neuroprotective effects against ischemic stroke (Joseph et al., Neuropharmacology, 81:134-141, 2014) . I intend to explore the mechanisms of these neuroprotective effects of C21 by focusing on potential anti-inflammatory actions of this agent in the brain after stroke. Specifically I will focus my studies on three inflammatory cell types; microglia, astrocytes, and invading T cells. The effects of cerebral ischemia on brain inflammation and on these cell types specifically following the activation of AT2Rs by C21 have not yet been explored, and my proposed studies will provide fundamental information about this. Such preclinical studies that employ new treatments are needed to justify the study of the protective renin-angiotensin system as a target for treating human stroke.".