How toxic proteins kill nerve cells in Alzheimer's patients' brains
Main Category: Alzheimer's / DementiaArticle Date: 16 Apr 2004 - 0:00 PDT
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Scientists have discovered how toxic proteins kill nerve cells in Alzheimer's patients' brains. The scientists hope their discovery will lead to new and more effective treatments for Alzheimer's patients.
You can read about this new research in the journal Science.
The accumulation of amyloid protein plagues is linked to Alzheimer's. According to findings in this new study, these plaques cause damage by interacting with an enzyme produced in the cell's energy-producing power plants.
This interaction damages the mitochondria, causing toxins to leak out, this causes the eventual destruction of the cell.
The scientists say that as the cells are lost so is memory and other symptoms associated with Alzheimer's.
The scientists analysed brain tissue from Alzheimer's patients as well as genetically engineered mice. The scientists say we should be able to, after some time, block or undermine the interaction between the amyloid plagues and the mitochondrial anzyme. Significant step
Dr Susanne Sorensen, Alzheimer's Society Research Head said "The link between the occurrence of amyloid plaques in the brain and the death of nerve cells has seemed obvious for many years, but there has been no clear experimental evidence for a mechanism that would explain how amyloid beta cause the death of nerve cells. This paper provides a possible explanation of how amyloid beta may cause cell death and points towards potential targets for drug therapy. This is very basic, but very important research. There is currently no real treatment for Alzheimer's disease that halts or reverses the disease."
The research team in this study came from various parts of the world.
Visit our alzheimer's / dementia section for the latest news on this subject.
MLA
15 Feb. 2012. <http://www.medicalnewstoday.com/releases/7318.php>
APA
http://www.medicalnewstoday.com/releases/7318.php.
Please note: If no author information is provided, the source is cited instead.
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