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Carlye Frisch

Hometown: Scottsdale, Arizona | Graduation Date: Spring 2020
Biomedical Engineering

Progerin-Induced Aging to Develop a Human-Induced Pluripotent Stem Cell Model of Alzheimer’s Disease

Mentor: David Brafman
FURI: Fall 2018

More than 5 million people currently live with Alzheimer’s Disease (AD), with no major life-extending treatment or cure. Reprogramming human-induced pluripotent stem cells (hiPSCs) resets the age to a fetal stage. Age-related phenotypes must be reintroduced into the DNA of the cells. Accumulation of the progerin protein is seen to be associated with aging. Using in-vitro techniques, it is hypothesized that the overexpression of progerin through a lentiviral system will artificially age hiPSC derived neurons to model Alzheimer’s Disease. Age-related phenotypes will be analyzed via immunofluorescence (IF) microscopy and mitochondrial superoxide assays, confirming the identity of the hiPSCs.

Other Projects

Progerin-Induced Aging to Develop a Human-Induced Pluripotent Stem Cell Model of Alzheimer’s Disease

Mentor: David Brafman
FURI: Spring 2018

Alzheimer’s Disease (AD) has the sixth highest mortality rate in the United States with no known cure or treatment. To model late-onset disorders, such as AD, age-related phenotypes must be reintroduced into the DNA of the cells. The accumulation of the progerin protein is associated with aging. Using in-vitro techniques, it is hypothesized that overexpressing progerin through the generation of a lentiviral system will artificially age human induced pluripotent stem cell (hiPSC) derived neurons to model AD. Age-related phenotypes in hiPSCs will be analyzed via immunofluorescence (IF) microscopy and mitochondrial superoxide assays to confirm the identity of the hiPSCs.