Sophia Velasco

Sophia Velasco

Mentor

Wolfgang J. Streit, Ph.D.

College

College of Medicine

Major

B.S. Chemistry (specialization: Biochemistry) & B.S. Psychology (specialization: Behavioral and Cognitive Neuroscience)

Minor

Pathogenesis & Classical Studies

Organizations

University of Florida Honors Program, Center for Undergraduate Research Board of Students (CURBS), Science Olympiad (National), Harvard Undergraduate Science Olympiad (HUSO) Online Initiative, Ambassadors of Liberal Arts and Sciences (CLAS)

Academic Awards

Florida Academic Scholar, William G. Nash Scholar (Fall 2020), University Scholars Program 2021-22, CLAS Dean’s List (Fall 2019-Present), Science Olympiad National Medalist (2019)

Volunteering

Science Olympiad Exam Author (National), HUSO Online Lecturer and Event Supervisor, Honors General Chemistry I/II Teaching Assistant, UFHealth Interdisciplinary Clinical and Academic (ICAP) Intern

Research Interests

Neurodegenerative diseases (Parkinson’s Disease, Alzheimer’s Disease, frontotemporal dementia), neuropathophysiology (ischemic stroke and diaschisis), and neurodevelopmental disorders (Fragile X Syndrome)

Hobbies and Interests

Avid plant collector, Taekwondo/martial arts, drawing, painting, and RPG video games

Research Project

Changes in axonal complexity, arborization, and networking of neurons harboring Xq27-q28 deletion due to Fragile X Syndrome

Fragile X Syndrome (FXS) is the most common form of inherited intellectual disability and common comorbid condition in people with autism. Patients that suffer from FXS present with severe behavior phenotypes, including hyperactivity, impulsivity, anxiety, poor language development, and seizures. In FXS, the amplification of the trinucleotide CGG repeat element within the 5’ of the FMR1 gene on the X chromosome causes a fragile site at the q arm. The FMR1 gene product, FMRP, is an RNA binding protein involved in regulating many mRNAs in human excitatory and inhibitory neurons. FMRP is also involved in normal dendritic spine development, maturation, and synaptic formation. Dendritic spines are critical components for excitatory synaptic networks and important for neuronal communications. The lack of FMRP in neurons also leads to the dysregulation of microtubule formation. As a consequence of microtubule dysregulation, the formation of dendritic spines is negatively affected and compromised. While animal models of FXS have provided valuable insight into the neurobiology of this condition, recent clinical trials based on animal models have failed to correct disease-related phenotypes in patients with FXS. These discrepant impacts of the loss of FMR1 function in mouse versus human brain and mouse versus human embryonic stem cells could be attributed to interspecies differences in brain development. In this project, we will test the hypothesis that iPSCs-derived cortical neurons harboring Xq27-q28 deletion exhibit a significant decrease in axonal complexity, dendritic arborization, and networking.

  • Wolfgang J. Streit, Ph.D.
  • B.S. Chemistry (specialization: Biochemistry) & B.S. Psychology (specialization: Behavioral and Cognitive Neuroscience)
  • Pathogenesis & Classical Studies
  • Neurodegenerative diseases (Parkinson’s Disease, Alzheimer’s Disease, frontotemporal dementia), neuropathophysiology (ischemic stroke and diaschisis), and neurodevelopmental disorders (Fragile X Syndrome)
  • Florida Academic Scholar, William G. Nash Scholar (Fall 2020), University Scholars Program 2021-22, CLAS Dean’s List (Fall 2019-Present), Science Olympiad National Medalist (2019)
  • University of Florida Honors Program, Center for Undergraduate Research Board of Students (CURBS), Science Olympiad (National), Harvard Undergraduate Science Olympiad (HUSO) Online Initiative, Ambassadors of Liberal Arts and Sciences (CLAS)
  • Science Olympiad Exam Author (National), HUSO Online Lecturer and Event Supervisor, Honors General Chemistry I/II Teaching Assistant, UFHealth Interdisciplinary Clinical and Academic (ICAP) Intern
  • Avid plant collector, Taekwondo/martial arts, drawing, painting, and RPG video games
  • Changes in axonal complexity, arborization, and networking of neurons harboring Xq27-q28 deletion due to Fragile X Syndrome
  • Fragile X Syndrome (FXS) is the most common form of inherited intellectual disability and common comorbid condition in people with autism. Patients that suffer from FXS present with severe behavior phenotypes, including hyperactivity, impulsivity, anxiety, poor language development, and seizures. In FXS, the amplification of the trinucleotide CGG repeat element within the 5’ of the FMR1 gene on the X chromosome causes a fragile site at the q arm. The FMR1 gene product, FMRP, is an RNA binding protein involved in regulating many mRNAs in human excitatory and inhibitory neurons. FMRP is also involved in normal dendritic spine development, maturation, and synaptic formation. Dendritic spines are critical components for excitatory synaptic networks and important for neuronal communications. The lack of FMRP in neurons also leads to the dysregulation of microtubule formation. As a consequence of microtubule dysregulation, the formation of dendritic spines is negatively affected and compromised. While animal models of FXS have provided valuable insight into the neurobiology of this condition, recent clinical trials based on animal models have failed to correct disease-related phenotypes in patients with FXS. These discrepant impacts of the loss of FMR1 function in mouse versus human brain and mouse versus human embryonic stem cells could be attributed to interspecies differences in brain development. In this project, we will test the hypothesis that iPSCs-derived cortical neurons harboring Xq27-q28 deletion exhibit a significant decrease in axonal complexity, dendritic arborization, and networking.