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Discovery may lead to Alzheimer’s cure
Written by Cassie Burica, Daily Vidette Reporter
Tuesday, 23 March 2010 20:44
 A new study suggests that a protein known for causing Alzheimer’s may actually be a natural defense against invading microbes and bacteria in the brain.
The protein, which is known as beta amyloid, or A-beta, forms into plaque that destroys signals between nerves. The buildup causes people to lose their memory and suffer from a personality change.
“It was thought that when these fragments accumulated and formed plaques, inflammation and damage killed off the neurons, resulting in the symptoms of Alzheimer’s disease,” Laura Vogel, professor of immunology, said
In a recent study, researchers at Harvard have suggested that the protein may actually have a useful function in defending the brain.
Upon looking at a list of genes that were associated with Alzheimer’s disease, Rudolph E. Tanzi, the lead researcher of the study, discovered that many resembled those associated with the innate immune system.
“Many cells and molecules in your body are part of the innate immune system, including neutrophils and macrophages that engulf and digest germs. Another important part of the innate immune system are small protein fragments called anti-microbial peptides.
“These are small molecules that exist all the time in your body so they are ready to attack pathogens the minute you get infected,” Vogel said.
 Tanzi and a colleague also discovered that A-beta closely resembled the protein LL-37, which has been known to protect against infections in rodents.
A-beta killed eight out of 12 of the microbes in an experiment, which is just as efficient, and in some cases more efficient at killing the microbes than LL-37.
Now that scientists understand that A-beta may actually be a necessary protein, the treatments may take a different route.
 Instead of Alzheimer’s being caused by A-beta, some scientists believe the disease is only caused by an excess of it.
“There could be significant clinical applications since many of the approaches to treat Alzheimer’s are trying to eliminate A-beta; if it turns out that you need A-beta to protect yourself from infection, getting rid of the protein may be a bad move,” Vogel explained.
H. Tak Cheung, professor of biology, explained that if the trigger of A-beta is a microorganism- based infection, controlling it may result in a cure.
“The extensive production of A-beta perhaps is the brain’s attempt to destroy a microorganism. So far we have not been able to find microorganisms in the brain using Alzheimer’s disease,” he said.
 “Maybe remnants of microorganisms that enter into the brain trick the brain to think it is infected by microorganisms and it responds in the production of A–beta.”
Cheung said that the discovery was similar to other medical breakthroughs in the past, such as the treatment of ulcers that were once thought to be only caused by stress but can now be treated with antibiotics.
“If this turns out to be correct, it could provide major importance to the treatment and cure of Alzheimer’s,” he said.
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