Date of Award

Winter 2026

Language

English

Embargo Period

1-15-2026

Document Type

Master's Thesis

Degree Name

Master of Science (MS)

College/School/Department

Department of Biomedical Sciences

Program

Biomedical Sciences

First Advisor

JoEllen Welsh

Second Advisor

Judy Narvaez

Committee Members

JoEllen Welsh, Doug Conklin, Ramune Reliene

Keywords

Alzheimer's disease, dementia, HT22 model

Subject Categories

Cell Biology | Medicine and Health Sciences | Nervous System Diseases

Abstract

Dementia is a crippling illness affecting millions worldwide causing significant public health burdens with long-term care. The lack of treatment options results in many years of suffering for affected individuals and their loved ones who often become primary caretakers. Decades of study have focused on treating dementia with little-to-no success, so an emphasis is needed on attempting to prevent disease progression altogether. This research explored vitamin K as a potential strategy for prevention of dementia onset or progression through the mechanism of suppressing ferroptosis. Ferroptosis is a type of cell death suggested to contribute to the hallmark traits of Alzheimer’s disease (the most common form of dementia), such as beta amyloid plaque buildup and tau aggregation. Targeting ferroptosis pathways that ultimately cause neurodegeneration has the potential to significantly lower the global burden of this disease. Understanding the mechanism of action of vitamin K in neuronal ferroptosis may lead to new non-toxic, easily implemented prevention strategies for dementia.

License

This work is licensed under the University at Albany Standard Author Agreement.

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