Air Pollution Contributes to Nearly 7 Million Premature Deaths Each Year, and Its Effects go far beyond the lungs. Breathing in Wildfire Smoke or Automobile-Related City does not just increase increase the risk of asthma and heart disease –T may also contribute to brain diseases as diversese as alzheimer ‘and autism.

Scientists at scripps research have discovered how a chemical change in the brain – health can be triggered by inflammation and aging as well as toxins found in air pollution, pesticides, bookfire smoke and processed Meats – Disrupts Normal Brain Cell Function. Known as S-Nitrosylation, this Chemical Change Prevents Brain Cells from Making New Connections and Ultimately Results in Cellular Death, The team discovered.

The research, published in the Proceedings of the National Academy of Sciences On February 27, 2025, Showed That Blocking S-Nitrosylation in a Key Brain Protein Partialy Reversed Signs of Memory Loss in Alzheimer’s Mouse MODELS and in NERVE Cells Produce Cells Produce Cells.

“We’ve Reveled The Molecular Details of how pollutants can contribute to memory loss and neurodegenerative disease,” Says Senior Author and Professor Stuart Lipton, MD, PH.D.D., PH.D., PH.D. Endowed Chair at Scripps Research and a Clinical Neurologist in La Jallla, California. “This could ultimately lead to new drugs that block these effects to better treatment alzheimer’s disease.”

More than two decades ago, lipton first discovered s-nitrosylation, a chemical process whereby a molecule related to nitric oxide (no) binds to sulfur (s) atoms within proteins (Producing “Snoi”) Their function and forming what lipton has called a “sno-storm” in the brain.

No is found naturally within the body and produced in response to electrical stimulation or inflammation-but it also (Designated PM2.5/No_x) Present in or triggered by Climate Change and Automobile-Related Air Pollution, Wildfire Smoke, Pesticides, and Processed Meats.

Lipton’s Research Group and Colleagues have previously demonstrated that Aberrant S-Nitrosylation Reactions Contribute to Some Forms of Cancer, Autis, Autis, Alzheimer’s Disease, Parakinson, Parakinson, Parakinsonsonsonsonsonsonson Other conditions.

In the new study, lipton’s group investigated the effect of s-nitrosylation on the protein Crtc1, which helps regulate genes that are critical for forming and maintales Essential process for learning and long-term memory.

Using Cultured Brain Cells from Mice and Humans, The Researchers First Confirmed that Excess No Leads to S-Nitrosylation of CRTC1. They then discovered that this chemical modification prevented Crtc1 from Binding to Another Critical Brain Regulatory Protein, Creb. As a result, other genes Necessary for Forming Connections Between Neurons Failed to Be Stimulated.

“This is a pathway that affects your memory and is directly implicated in human alzheimer’s disease,” Says lipton.

Indeed, The team observed high levels of s-nitrosylated Crtc1 at an early stage of disease in alzheimer’s mouse models and in human neurons derived from stem cells of alzhemers, Supporting the idea that the chemical change plays a key role in the development of disease symptoms.

Next, The Research Team Genetically Engineered A Version of Crtc1 that Cold No Longer Undergo S-Nitrosylation, as the Protein Now Lacked The Sulfur-Constaining Acid For the chemical reaction. In a petri dish, introducing this modified version of Crtc1 Into Human Nerve Cells Derived from Alzheimer’s PATENT STM CELLS Prevended Signs of Disease, Including of Nereve COLLL KONNATIONS and NECRASED NERVE Cell Survival.

In Alzheimer’s mouse models, the re-enginered CRTC1 restored the activation of genes required for memory formation and synaptic plasticity-thee brain’s ability to strengthen connections belong

“Weound Nearly Completely Rescue Molecular Pathways Involved In Making New Memories,” Says lipton. “It sugges that this is a druggable target that could make a real difference in treatment alzheimer’s and potentially other neurological diseases.”

Given that environmental toxins, include automobile pollution and wildfire smoke, can result in elevated no levels in the brain, the new student strengthens the hypothenes the hypothesis Aging and alzheimer’s through s-nitrosylation. Preventing S-Nitrosylation of Crtc1 could be a viable pathway towing or preventing this type of alzheimer’s-Related Brain Damage, Says Lipton.

The findings may also help explain why alzheimer’s risk increases with age, he adds. Even without Exposure to Environmental toxins, Aging Leads to Increased Inflammation and Higher No Levels, While The Body’s Anti’s Antioxidant Defenses Weaken -Making Proties More Suseptiles to harmful S-nitrosylation reactions.

“We’re learning that s-nitrosylation affects numerous proteins throughout the body, but reveresing just some of these changes-like that on Crtc1-COULD HAVE A Significant Function, “Explains Lipton.

His research group is now working to develop drugs that can selectively block certain s-nitrosylation reactions, Including the Affecting Crtc1.