Journal of Undergraduate Research
Alzheimer’s Disease: A New Model Defining the Mechanism of Iron- Catalyzed Radical Damage to Neurons
Keywords
Alzheimer's disease, mechanism of iron-catalyzed radical damage
College
Physical and Mathematical Sciences
Department
Chemistry and Biochemistry
Abstract
The MEG proposal focused on understanding how elevated homocysteine levels cause the inability of cells to control iron levels as a cause for Alzheimer’s disease. Iron is associated with the amyloid plaques and tau tangles that are proposed to cause damage to neurons. Dr. Wisco and I previously submitted an NIH R15 proposal that was viewed positively but was not funded due to a lack of preliminary data. Our goal was to use MEG funding to provide preliminary data supporting the hypothesis. We proposed that Homocysteine was a dangerous trigger for disrupting iron metabolism. Biochemical techniques, immunohistochemistry techniques and MRI were used in animal models and cell culture models to test the hypothesis that Homocysteine disrupted iron metabolism and leads to accumulation in amyloid plaques and tau tangles. The starting of the mice colony took awhile to get started so many of the results are still in process of being obtained. We are currently studying the 6 month mice of a 1 year experiment.
Recommended Citation
Watt, Richard and Wisco, Jonathan
(2017)
"Alzheimer’s Disease: A New Model Defining the Mechanism of Iron- Catalyzed Radical Damage to Neurons,"
Journal of Undergraduate Research: Vol. 2017:
Iss.
1, Article 343.
Available at:
https://scholarsarchive.byu.edu/jur/vol2017/iss1/343