The sticky plaques in the brain which scientists believed caused Alzheimer's disease may in fact be fighting an underlying infection, a new study suggests.
Researchers have discovered that clumps of beta-amyloid protein, which are seen in the brains of people suffering dementia, actually form part of the immune system.
The protein appears to protect against lethal infections, such as salmonella.
Mice genetically engineered to produce the protein survived significantly longer after their brains were infected by salmonella than normal mice.
The discovery could provide an explanation for why drugs which target the protein have never worked to reverse or slow down the progression of Alzheimer's disease.
Dr Robert Moir, from Massachusetts General Hospital in the US, said: “Neurodegeneration in Alzheimer's disease has been thought to be caused by the abnormal behaviour of A-beta molecules, which are known to gather into tough fibril-like structures called amyloid plaques within patients' brains.
“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.”
The new study is the first to investigate the anti-microbial action of human beta-amyloid in living animals.
Scientists believe that it may be the ability of the protein to from clumps that makes it so effective against infection. The clumping is thought to kill microbes by breaking down their cell walls.
Dr Moir added: “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.
“It does appear likely that the inflammatory pathways of the innate immune system could be potential treatment targets.
“If validated, our data also warrant the need for caution with therapies aimed at totally removing beta-amyloid plaques. Amyloid-based therapies aimed at dialling down but not wiping out beta-amyloid in the brain might be a better strategy.”
The research is published in the journal Science Translational Medicine