Alzheimer disease is a major age-associated neurodegenerative disorder affecting a large percentage of the U.S. population over the age of 70. There are no effective therapies to cure or prevent it, largely due to a lack of understanding of the pathophysiology of the disorder. Although there are some known genetic predispositions to develop AD, the vast majority of cases are sporadic. The causes are multifactorial, but one major contributing factor that has garnered the attention of researchers in recent years is the cumulative damage from increased production of reactive oxygen species (ROS), which include superoxide (O2-) and peroxynitrite (ONOO-), on synapses in the brain that lead to neuron loss. A review article from 2017 gives some background information on the pathophysiology of AD and the purported links to ROS production:
http://doi.org/10.3233/JAD-161088Links to an external site.
(the above article is open access)
Based on the information presented in this article, and from any other sources that you might be able to locate, please address the following questions in your response:
What are reactive oxygen species, where do they come from, and how do they contribute to the pathophysiology of AD?
What is the normal physiological role of ROS in the body? Are they necessarily harmful to cells? Why or why not?
Identify at least one specific example of ROS-induced damage that can lead to synaptic dysfunction and the development of AD. How is the protein or structure that you identified affected by ROS?