New study explores air pollution's link to Alzheimer's
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New Delhi: Toxins from air pollution and wildfire smoke may trigger a chemical change in the brain, leading to memory loss associated with Alzheimer's disease, a new study suggests.
Researchers at Scripps Research in the US have made a discovery, identifying a specific chemical change known as S-nitrosylation, which plays a crucial role in disrupting the ability of brain cells to form new connections, ultimately leading to cellular death.
Blocking S-nitrosylation led to a partial reversal of memory loss symptoms in mouse models of Alzheimer's disease, as well as in human nerve cells derived from stem cells.
"We've revealed the molecular details of how pollutants can contribute to memory loss and neurodegenerative disease," said Stuart Lipton, professor at Scripps Research.
"This could ultimately lead to new drugs that block these effects to better treat Alzheimer's disease," Lipton added.
The study's findings have been published in the Proceedings of the National Academy of Sciences. Dr. Lipton's research group and collaborators have previously established a link between abnormal S-nitrosylation reactions and various diseases, including certain types of cancer, autism, Alzheimer's, Parkinson's, and other conditions.
In their latest study, Dr. Lipton and his team explored the impact of S-nitrosylation on the protein CRTC1, a key regulator of genes essential for the formation and maintenance of connections between brain cells.
The researchers began by using cultured brain cells from both mice and humans to demonstrate that excessive levels of nitric oxide (NO) trigger S-nitrosylation of the CRTC1 protein. Further investigation revealed that this chemical alteration hindered CRTC1's ability to interact with CREB, a crucial regulatory protein in the brain.
As a result, other genes necessary for forming connections between neurones failed to be stimulated.
"This is a pathway that affects your memory and is directly implicated in human Alzheimer's disease," said Lipton.
The team detected abnormally high levels of S-nitrosylated CRTC1 in both mouse models of Alzheimer's disease and human neurones generated from patient stem cells, even in the early stages of the disease.
The findings further support the idea that chemical change plays a key role in the development of disease symptoms.
(inputs from IANS)