Brain destruction in Alzheimer's disease is caused by the build-up of a protein called amyloid beta in the brain, which triggers damaging inflammation and the destruction of nerve cells. One in three people who live to be over 65 will end their lives with a form of dementia. 700,000 people in the UK have a form of dementia, more than half have Alzheimer's disease. In less than 20 years nearly a million people will be living with dementia. This will soar to 1.7 million people by 2051. 1 in 6 people over 80 have dementia.
Scientists had previously shown that preventing individual amyloid beta proteins from sticking to one another minimized brain lesions and protected nerve cells against damage.
The new study - a collaborative effort by researchers in Germany and the US - shows that an anti-inflammatory drug (called CNI-1493) may have the same effect. The drug - already tested in humans for the treatment of inflammatory diseases - protected nerve cells against amyloid beta-induced damage in culture. In mice prone to developing an Alzheimer's-like disease, the drug decreased brain inflammation and improved memory and cognitive function.
Other anti-inflammatory drugs, such as ibuprofen, have been shown to reduce Alzheimer's disease lesions in the brains of rodents, but CNI-1493 appears to be faster and more effective. If these results hold up in humans, CNI-1493 may provide a more effective alternative to current Alzheimer's therapies, which temporarily prolong the function of nerve cells but do not prevent their destruction. ...http://www.medicalnewstoday.com
posted by Valery Yermalitsky at
6:22 AM
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