Studying ROS release in response to protein polymorphism in PC-12 cells

Presenter's Name(s)

Uma Nudurupati

Abstract

Senile plaques, a hallmark of Alzheimer's disease, primarily contain the amyloid beta (Aβ) protein in fibrillar form. These fibrillar forms can take on different structures, called polymorphs of Aβ. There has been a great deal of debate on what the cytotoxic forms of Aβ is, whether it is fibril polymorphs or oligomers. There is evidence that different polymorphs are correlated with different severity of symptoms in patients. There is evidence that oligomers may be the most toxic form. It is known that amyloids can produce reactive oxygen species (ROS) and generate oxidative stress, which promotes cellular cytotoxicity. A comprehensive understanding of the relationship between Aβ structural polymorphs, oligomers, and the corresponding induced cellular ROS released is lacking. In this talk, we will discuss studies in which we electrochemically measure ROS released from model neuronal cells (Rat Pheochromocytoma Cells, PC-12 cells) when treated with a suite of protein polymorphs, and oligomers, across varying strengths and evaluate their impact on the cells’ viability.

Primary Faculty Mentor Name

Yangguang Ou

Status

Graduate

Student College

College of Arts and Sciences

Program/Major

Chemistry

Primary Research Category

Physical Science

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Studying ROS release in response to protein polymorphism in PC-12 cells

Senile plaques, a hallmark of Alzheimer's disease, primarily contain the amyloid beta (Aβ) protein in fibrillar form. These fibrillar forms can take on different structures, called polymorphs of Aβ. There has been a great deal of debate on what the cytotoxic forms of Aβ is, whether it is fibril polymorphs or oligomers. There is evidence that different polymorphs are correlated with different severity of symptoms in patients. There is evidence that oligomers may be the most toxic form. It is known that amyloids can produce reactive oxygen species (ROS) and generate oxidative stress, which promotes cellular cytotoxicity. A comprehensive understanding of the relationship between Aβ structural polymorphs, oligomers, and the corresponding induced cellular ROS released is lacking. In this talk, we will discuss studies in which we electrochemically measure ROS released from model neuronal cells (Rat Pheochromocytoma Cells, PC-12 cells) when treated with a suite of protein polymorphs, and oligomers, across varying strengths and evaluate their impact on the cells’ viability.