Scientists May Have Been Fighting Alzheimer's Wrong For The Last 30 Years Suggests Study

Symptoms could actually be our immune system fighting a hidden infection.

A controversial study has suggested that the sticky plaques in the brain which are believed to be causing Alzheimer's disease could in fact be a natural part of our immune system.

People who have dementia all suffer from a buildup of beta-amyloid protein in the brain. It's believed that this buildup then eventually blocks the synapses from communicating with each other leading to increased loss of brain function.

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Well now it's believed that this beta-amyloid protein could in fact be actually trying to combat an underlying infection.

Scientists at Massachusetts General Hospital found that mice who were producing the human version of beta-amyloid proteins were able to fight off salmonella far more efficiently than mice without it.

While the clumping of proteins has traditionally been seen as a negative sign it's now thought that this process is in fact the body's immune system trying to break down microbe cell walls that are attacking the brain.

Amyloid plaques, that may damage and kill neurons by generating reactive oxygen species during its self-aggregation.
Amyloid plaques, that may damage and kill neurons by generating reactive oxygen species during its self-aggregation.
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Dr Robert Moir, from MGH in the US points out that if true this would require a completely new approach to fighting Alzheimer's Disease.

"This widely held view 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."

If true it would mean that future treatments should not be focused on completely removing beta-amyloid protein from the brain as it could in fact be the one thing that's trying to fight off a previously unseen infection.

Instead treatments would find the root microbes, target that and then work on reducing but not eliminating beta-amyloid protein from the brain.

Scientists in the field have put forward their skepticism over the research however, suggesting that further study on human patients is needed before this 'proof of concept' can be totally proved accurate.

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