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Alzheimer's disease may be the result of infection, Harvard study suggests

by , 29 August 2017
Alzheimer's disease may be the result of infection, Harvard study suggests
For many years, scientists have believed that the plaques known as amyloid beta that collect in the brains of people with Alzheimer's disease serve no purpose, and that their presence does nothing but rob people of their minds and memories.

However, a new study by Harvard researchers published in the journal Science Translational Medicine suggests that the plaques may have a role after all, potentially in staving off infection, and that Alzheimer's disease may be the devastating result of this real purpose. Read on for the full story…

Study finds that the purpose of amyloid beta may be to fight off infection

The study was led by Robert Moir of the Genetics and Aging Research Unit at the MassGeneral Institute for Neurodegenerative Disease in Boston who’s also an assistant professor of neurology at Harvard Medical School in Massachusetts, both in the United States.
This study was a follow-up to a 2011 study in which Moir and his team demonstrated that amyloid beta could kill pathogens such as candida in test tubes. For this new study, the researchers took the idea a step further, not quite to humans, but to living organisms including mice, round worms and fruit flies.
The team found that the creatures that they genetically engineered to produce high levels of amyloid beta were able to fight off infections from salmonella and other microorganisms more successfully than those with low levels. “The really surprising thing was it doesn’t just kill microbes like an antibiotic,” explained Moir.


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Instead, amyloid beta use exactly the same structure that’s the hallmark of Alzheimer’s disease to entomb the offenders. The team noted that the plaques did this quickly – and they didn’t let go. “The good side is the bugs don't get out, but it's very hard for us to clear the amyloid,” said Moir.
The team hypothesized that more bugs are able to cross the blood-brain barrier as we age, which triggers our entire system into overdrive. In simpler terms, low-level chronic inflammation and the inflammation and immune response that go with it may be culprits in Alzheimer’s disease.

Alzheimer’s disease hasn’t seen a new drug approval since 2003!

This new study could change the way we think of Alzheimer’s disease – a disease that hasn’t seen a new drug approval since 2003. It may even change stubborn scientists’ efforts to both treat and understand it.
That said, any practical applications of this new research are still a long way off. “It's intriguing, it's exciting, and it opens new opportunities for intervening in the disease, but at the same time it's very preliminary and speculative,” commented Ronald Petersen, director of the Mayo Clinic Alzheimer’s Disease Research Center in Minnesota in the United States. “I wouldn't go too far in saying that this is the answer or breakthrough.”
Keep your eyes peeled for further news on this new discovery about Alzheimer’s disease!

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