Michael Strickland

Mentor: Dr. Paramita Chakrabarty
College of Medicine
"The reason that I got involved with research has been my longstanding interest in biology and in neuroscience specifically. Reading Carl Sagan's "A Demon Haunted World" greatly influenced my love of science and that science should be used as a tool to improve the lives of others and society at large. My research in neurodegenerative diseases allows me to combine the study of basic science with the goal of directly improving the lives of those who suffer from diseases such as ALS, Alzheimer's, and Parkinson's Disease."


Biochemistry, Systems Biology



Research Interests

  • Neuroscience
  • Neurodegenerative Diseases
  • Systems Biology

Academic Awards

  • International Baccalaureate Diploma 2013
  • Bright Futures Scholarship 2013
  • University Scholars Program 2016


  • Humanists on Campus
  • Gator Freethought



Hobbies and Interests

  • Backpacking
  • Camping
  • Traveling
  • Reading

Research Description

Chemokine Based Immunobiotherapeutics in ALS
Amyotrophic Lateral Sclerosis (ALS) is a neurodegenerative disease that results in motor neuron degeneration in the spinal cord eventually leading to paralysis and death. It is not known what causes ALS, however, research suggests that neuroinflammation plays a key role in disease pathogenesis and progression. The therapeutic approach our project tests involves the use of decoy chemokine receptors that are capable of scavenging inflammatory chemokines, pro-inflammatory cytokines, which are associated with ALS. It is believed that by modulating the immune response in this way, vulnerable neuronal populations will experience less stress as a result of a reduced immune response and that there will be less neuroinflammation and neurodegeneration. The two main objectives of the project are to (1) determine the efficacy of decoy chemokine receptors (D6, M3, and DARC) in delaying the onset of ALS pathology in SODG93A neonatal mice and (2) to determine the effect of introducing inflammatory chemokines (Ccl2, Ccl3, and Ccl5) which is expected to promote disease progression in neonatal mice if our hypothesis is correct.