This project attempts to better understand how the WNT transcriptional program is affected by β-catenin and SP5 by developing an in vitro model of neural patterning. This signaling pathway uses molecules that mediate cell to cell communication, which controls fundamental embryonic processes and regulates the formation of developmental markers. In the absence of WNT, the
Navajo Neurohepatopathy (NNH) is caused by a single nucleotide polymorphism (SNP) and is fatal to the 1 in 1,600 Navajo children affected. To confirm positive NNH diagnoses, clinicians need to collect genetic samples noninvasively from the child and the mother (who would be a carrier if the child has NNH). Therefore, this study aimed to
A live method to test the functionality of cell culture and tissue is needed to assess the growth of cells for further in-line applications. Fluorescent oxygen sensing siloxane nanoprobes provide the opportunity to do so. The project aims to optimize the method of labeling different cell types and cultures, such as neural progenitor cells(NPCs), neurons,
Navajo Neurohepatopathy (NNH) is a fatal genetic disease that impacts 1 in every 1,600 Navajo children below the age of ten. This disease is caused by a single nucleotide polymorphism (SNP) within the MPV17 gene. Current standard of care requires sequencing of the entire MPV17 gene, which costs $700 per patient and takes three weeks
Alzheimer’s disease (AD) is one of the top leading causes of death in the U.S. Cell therapies for AD using neural progenitor cells (NPC) have been tested, but it is unknown if they are safe and efficient once inside the body. By developing an effective cell labeling method utilizing siloxane-based nanoprobes that allows for the
Alzheimer’s Disease (AD) affects over 5 million individuals in the US. The idea behind selective cell vulnerability in AD and various amyloid-dependent have been postulated. However, such mechanistic studies do not consider all the aspects of the human disease. This research leverages the ability for the generation of neural cell types of various regional identities
The caveat of using a human induced pluripotent stem cell (hiPSC) model for studying any late onset age progressive disorder like Alzheimer’s Disease (AD), is the loss of age-associated makers as a result of reprogramming. Progerin is the protein responsible for premature aging in Progeria and it can be used to artificially age the cells.
Developing a method to turn stem cells into neurons in large quantities can help with the study of Alzheimer’s disease.
Studying the aging mechanism of pluripotent stem cells will help better model age-related Alzheimer’s disease.
Using CRISPR to age model neurons for Alzheimer’s disease study will lead to better understanding and treatments.