Although the majority of Alzheimer’s Disease (AD) cases are idiopathic, multiple genetic risk variants have been identified, the most powerful and prevalent of which is the E4 variant of Apolipoprotein E (APOE) gene. Interestingly, individuals harboring a copy of the E2 variant of APOE show ~40% decrease in lifetime risk of developing AD compared to individuals with an APOE 3/3 genotype. Amyloid-dependent and -independent mechanisms have been postulated to explain the APOE4 gain of toxic effect, however the mechanism by which APOE2 modulates AD disease risk, especially during aging, remains unclear. To that end, I have established a diverse set of human induced pluripotent stem cell (hiPSC) lines from AD and non-demented control (NDC) patients with no (i.e. APOE 3/3) and two (i.e. APOE 4/4) copies of the E4 allele. Using novel genome editing techniques I am generating sets of isogenic APOE2 hiPSC lines to elucidate the potential genetic, molecular, and cellular mechanisms by which the APOE2 allele confers a protective effect on AD onset and age-related progression.
Although my current work focuses on disease modeling, my future career goals are centered around the clinical translation of stem cell therapies. The regenerative medicine applications of hiPSCs are numerous, and I hope to be on the forefront of translational stem cell research aimed at treating neurodegenerative diseases.
I entered the CTS Ph.D. program in Fall 2016 after earning my B.Sc. in Bioengineering at the University of California - San Diego.
Faculty mentors: Dr. David Brafman (Arizona State University) and Dr. Ron Hammer