While the connection between air pollution and lung disease could appear obvious, the link between breathing in toxins and suffering memory loss looks about as clear as a cloud of cigarette smoke.
Scientists at Scripps Research Institute first identified how contaminants in smog, pesticides, and other airborne chemical can affect the brain. Now they have identified a way to potentially reverse those effects, they report in the Proceedings of the National Academy of Sciences.
Learning About Memory Loss
A chemical process in the brain called S-nitrosylation — which can be activated by inflammations as well as a variety of airborne toxins — blocks brain cells from making new connections, leading to brain cell death, then memory loss. Blocking S-nitrosylation in a specific brain protein partially reverses memory loss in mouse models for Alzheimer’s disease.
“We’ve revealed the molecular details of how pollutants can contribute to memory loss and neurodegenerative disease,” Stuart Lipton, a Scripps neuroscientist and an author of the study, said in a press release. “This could ultimately lead to new drugs that block these effects to better treat Alzheimer’s disease.”
Read More: What You Need to Know About the 6 Stages of Alzheimer’s Disease
Brain Chemistry Connections
Lipton first discovered S-nitrosylation about two decades ago. In that chemical process, a molecule related to nitric oxide (NO) binds to sulfur (S) atoms within proteins. That process alters brain function. While the body produces NO in response to electrical stimulation or inflammation, it also arises in response to particulate matter associated with several types of air pollution. His team has previously demonstrated that S-nitrosylation gone awry can contribute to some forms of cancer, autism, Alzheimer’s disease, and other conditions.
In the new study, Lipton’s group first investigated how S-nitrosylation affected a protein associated with creating connections between brain cells. After confirming that excess NO indeed triggers S-nitrosylation, they showed how those chemical changes interfere with other brain proteins essential for memory. They then engineered a protein that resisted the S-nitrosylation process associated with memory loss — first in a petri dish, then in a mouse model.
“We could nearly completely rescue molecular pathways involved in making new memories,” Lipton said. “It suggests that this is a druggable target that could make a real difference in treating Alzheimer’s and potentially other neurological diseases.”
Read More: The 4 Main Types of Dementia
Restoring Memory
Studies have already established that environmental toxins lead to higher NO levels in the brain. The new work strengthens the hypothesis that these toxins can accelerate brain aging and Alzheimer’s through S-nitrosylation.
Therefore, preventing that process in critical brain proteins could slow or prevent brain damage in Alzheimer’s patients. The group is now developing drugs to block key S-nitrosylation reactions.
Article Sources
Our writers at Discovermagazine.com use peer-reviewed studies and high-quality sources for our articles, and our editors review for scientific accuracy and editorial standards. Review the sources used below for this article:
Proceedings of the National Academy of Sciences. S-Nitrosylation of CRTC1 in Alzheimer’s disease impairs CREB-dependent gene expression induced by neuronal activity
Before joining Discover Magazine, Paul Smaglik spent over 20 years as a science journalist, specializing in U.S. life science policy and global scientific career issues. He began his career in newspapers, but switched to scientific magazines. His work has appeared in publications including Science News, Science, Nature, and Scientific American.
