Mitochondrial Damage by Amyloid-Beta in Alzheimer鈥檚 Disease
By Dr. Deguo Du, Dr. Yunqing Kang, and Dr. Ewa Wojcikiewicz
Keywords: Alzheimer鈥檚 disease, dementia, amyloid-beta, mitochondria, membrane, molecular biology, neurodegeneration, neuroscience, therapeutic research
Our Research
Alzheimer鈥檚 disease causes memory loss and cognitive decline. One key factor is the buildup of a protein fragment called amyloid-beta (A尾), which can harm brain cells. While traditionally studied outside cells, A尾 also clumps inside cellular structures like mitochondria, which produce energy for cells.
Our research investigates how A尾 interacts with mitochondria and causes early cell damage. We focus on the protein鈥檚 N-terminal region, which may help it stick to membranes and form harmful clumps. Understanding this process can point toward new ways to prevent or slow Alzheimer鈥檚 progression.
Our Strategy
Students will learn and contribute to:
- Buildup of mitochondrial membrane mimics to test how A尾 binds and aggregates
- Biochemical and biophysical methods to monitor protein clumping and membrane disruption
- Testing peptide-based strategies designed to block A尾鈥搈embrane interactions
- Computational approaches to predict molecular interactions
- Data analysis and interpretation of biochemical and cellular results
This hands-on research teaches skills in molecular biology, experimental design, and problem-solving while exploring a pressing health challenge.
Our Impact
By uncovering the early steps of A尾 toxicity, this work may:
- Lead to new targets for therapies
- Help prevent or delay cognitive decline in Alzheimer鈥檚 patients
- Improve understanding of mitochondrial health in neurodegenerative diseases
This project contributes to better prevention and treatment strategies for Alzheimer鈥檚 and related dementias.
Our Team