New Delhi, March 1 (IANS) Toxins found in air pollution, and wildfire smoke may trigger a chemical change in the brain that can lead to memory loss as seen in Alzheimer’s disease, according to a study.
Scientists at Scripps Research, US, discovered a chemical change — known as S-nitrosylation — that prevents brain cells from making new connections and ultimately results in cellular death.
Blocking S-nitrosylation partially reversed signs of memory loss in Alzheimer’s mouse models and nerve cells produced from human 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 findings are published in the journal Proceedings of the National Academy of Sciences. Lipton’s research group and colleagues have previously demonstrated that aberrant S-nitrosylation reactions contribute to some forms of cancer, autism, Alzheimer’s disease, Parkinson’s disease, and other conditions.
In the new study, Lipton and team investigated the effect of S-nitrosylation on the protein CRTC1, which helps regulate genes that are critical for forming and maintaining connections between brain cells.
Using cultured brain cells from mice and humans, the researchers first confirmed that excess nitric oxide (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,” said Lipton.
In both the Alzheimer’s mouse model and in human neurons derived from stem cells of patients with the neurodegenerative condition, the team observed high levels of S-nitrosylated CRTC1 at an early stage of the disease.
The findings further support the idea that chemical change plays a key role in the development of disease symptoms.
–IANS
rvt/
Disclaimer
The information contained in this website is for general information purposes only. The information is provided by TodayIndia.news and while we endeavour to keep the information up to date and correct, we make no representations or warranties of any kind, express or implied, about the completeness, accuracy, reliability, suitability or availability with respect to the website or the information, products, services, or related graphics contained on the website for any purpose. Any reliance you place on such information is therefore strictly at your own risk.
In no event will we be liable for any loss or damage including without limitation, indirect or consequential loss or damage, or any loss or damage whatsoever arising from loss of data or profits arising out of, or in connection with, the use of this website.
Through this website you are able to link to other websites which are not under the control of TodayIndia.news We have no control over the nature, content and availability of those sites. The inclusion of any links does not necessarily imply a recommendation or endorse the views expressed within them.
Every effort is made to keep the website up and running smoothly. However, TodayIndia.news takes no responsibility for, and will not be liable for, the website being temporarily unavailable due to technical issues beyond our control.
For any legal details or query please visit original source link given with news or click on Go to Source.
Our translation service aims to offer the most accurate translation possible and we rarely experience any issues with news post. However, as the translation is carried out by third part tool there is a possibility for error to cause the occasional inaccuracy. We therefore require you to accept this disclaimer before confirming any translation news with us.
If you are not willing to accept this disclaimer then we recommend reading news post in its original language.