Research Investigates Link Between Air Pollution and Alzheimer's Memory Loss
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Synopsis
A study reveals that toxins from air pollution and wildfire smoke can cause biochemical changes in the brain, leading to memory loss associated with Alzheimer's disease. Researchers at Scripps Research found that these changes, specifically S-nitrosylation, impact crucial brain proteins and could be targeted for new treatments.
Key Takeaways
- Toxins in air pollution may affect brain function.
- S-nitrosylation is a key chemical alteration linked to memory loss.
- Research may lead to new Alzheimer's treatments.
- Protein CRTC1 plays a role in neuron connection regulation.
- High S-nitrosylated CRTC1 levels observed in early Alzheimer's stages.
New Delhi, March 1 (NationPress) Harmful substances present in air pollution and wildfire smoke may instigate a biochemical alteration in the brain, leading to memory degradation similar to that observed in Alzheimer's disease, according to recent research.
Researchers at Scripps Research, USA, identified a biochemical alteration known as S-nitrosylation, which inhibits brain cells from forming new synaptic connections, ultimately leading to cell death.
Inhibiting S-nitrosylation showed partial reversal of memory loss symptoms in mouse models of Alzheimer's, as well as in nerve cells created from human stem cells.
"We have uncovered the molecular intricacies of how pollutants may lead to memory impairment and neurodegenerative disorders," stated Stuart Lipton, a professor at Scripps Research.
"This research could pave the way for novel medications that counteract these effects, improving treatment options for Alzheimer's disease," Lipton further remarked.
The study's results are documented in the journal Proceedings of the National Academy of Sciences. Lipton's research team has previously established that irregular S-nitrosylation processes contribute to various illnesses, including some cancers, autism, Alzheimer's, Parkinson's disease, and more.
In this latest investigation, Lipton and his team examined the influence of S-nitrosylation on the protein CRTC1, which is essential for regulating genes crucial for forming and sustaining synaptic connections between neurons.
Utilizing cultured brain cells from both mice and humans, the researchers initially validated that excess nitric oxide (NO) induces S-nitrosylation of CRTC1. They subsequently found that this chemical alteration hindered CRTC1 from interacting with another vital regulatory protein in the brain, CREB.
Consequently, other genes necessary for establishing neuronal connections were not adequately activated.
"This pathway significantly impacts memory and is directly associated with human Alzheimer's disease," Lipton commented.
In both the Alzheimer's mouse model and human neurons derived from stem cells of patients with this neurodegenerative condition, the team noted elevated levels of S-nitrosylated CRTC1 during the early stages of the disease.
The findings further bolster the notion that this biochemical alteration is instrumental in the emergence of disease symptoms.
