Over four million individuals in the United States currently suffer from Alzheimer's disease (AD), a devastating disorder of progressive dementia. Within the next several decades, AD is expected to affect over 22 million people globally. AD can only be definitively diagnosed by postmortem examination. Thus, investigation into the specific pathogenesis of neuronal degeneration and death in AD on a biochemical level is essential for both earlier diagnosis and potential treatment and prevention options. Overproduction of amyloid [3-peptide (A[3) in the brain leads to both free radical oxidative stress and toxicity to neurons in AD. My undergraduate biochemical studies with regard to AD explore the various ways in which free radical oxidative stress might contribute to the pathology of AD. In particular, this review highlights studies using Af3-precursor mutations in animal models, and analysis of histone-DNA interactions.
"The Role of Oxidative Stress in Alzheimer's Disease,"
Vol. 2, Article 15.
Available at: http://uknowledge.uky.edu/kaleidoscope/vol2/iss1/15