• Scientists have linked a protein known to cause Alzheimer's disease to brain infections. (Google)Source: Google
Research suggests that the protein thought to play a role in causing Alzheimer’s disease may be a part of our immune system.
By
Jody Phan

27 May 2016 - 1:34 PM  UPDATED 27 May 2016 - 1:34 PM

A protein called amyloid beta was thought of as the waste product which clumps into plaques in the brains of Alzheimer’s sufferers, destroying nerve connections and memory.

But a new study at Harvard Medical School and Massachusetts General Hospital suggests that the protein is a by-product of the brain’s immune reaction to infection.

The study, published in Science Translational Medicine, could change how researchers look at the protein and the development of medicines used to treat the condition.

The negative view of these amyloid beta protein clusters “has guided therapeutic strategies and drug development for more than 30 years, but our findings suggest that this view is incomplete.”

The researchers hypothesised that amyloid beta protein forms a protective cage around viral, bacterial and fungal infections in the brain, causing the infection to die. What remains is the plaque, which is the hallmark of Alzheimer’s disease.

They used mice and roundworms to test the theory and found that mice genetically modified to produce high levels of amyloid beta protein survived twice as long as those that didn’t have the protein when infected with a strain of salmonella.

Meanwhile, roundworms infected by the Candida albicans fungus survived twice as long with the presence of the amyloid beta protein.


If the clumping of amyloid beta proteins is how the body fights pathogens attacking the human brain, researchers believe it would completely change the approach to fighting Alzheimer’s disease.

"Our findings raise the intriguing possibility that Alzheimer's pathology may arise when the brain perceives itself to be under attack from invading pathogens."

Dr Robert Moir, one of the researchers in the study, says the negative view of these amyloid beta protein clusters “has guided therapeutic strategies and drug development for more than 30 years, but our findings suggest that this view is incomplete".

"Our findings raise the intriguing possibility that Alzheimer's pathology may arise when the brain perceives itself to be under attack from invading pathogens, although further study will be required to determine whether or not a bona fide infection is involved,” he said in a press release.

Dr Rudolph Tanzi told Scientific American that instead of trying to eliminate the amyloid beta protein, those researching the treatment of Alzheimer’s disease should focus on ways to lower the levels.

“We might want to think about just dialling it down,” he says.

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