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Alzheimer鈥檚 disease may be caused by the abnormal build-up of a protein in the gut that gradually spreads to the brain, according to research in mice.

In people with Alzheimer鈥檚 disease, a protein called beta-amyloid clumps together in the brain to form plaques that disrupt normal brain processes. Beta-amyloid deposits have also been found in the guts of people who died with the condition, but they have been largely overlooked.

John Rudd at the Chinese University of Hong Kong and his colleagues wondered if the beta-amyloid found in the brains of people with Alzheimer鈥檚 disease may originally have come from their guts.

To test this idea, the researchers injected small amounts of the protein into the gastrointestinal tracts of mice. The beta-amyloid had a fluorescent marker attached so they could see where it ended up.

The protein was rapidly taken up by the complex cluster of neurons that line the guts, which are sometimes referred to as the body鈥檚 鈥�second brain鈥�. One year later, the beta-amyloid had migrated up the vagus nerve, which connects the gut and the brain, and into the brains of the mice.

After the beta-amyloid entered the brains, the mice displayed short-term and long-term memory problems reminiscent of those seen in people with Alzheimer鈥檚 disease.

The exact role beta-amyloid in the brain plays in causing Alzheimer鈥檚 symptoms is still unclear, but if the protein is migrating from the gut in people, it may be possible to prevent or delay the condition by removing beta-amyloid before it spreads to the brain, says Rudd. 鈥淓ven if only some of the beta-amyloid load in the brain comes from the gastrointestinal tract, stopping or slowing that could give people an extra one or two years,鈥� he says.

Bryce Vissel at the University of Technology Sydney in Australia says the idea is plausible, but needs more evidence to back it up. 鈥淎lzheimer鈥檚 disease can probably be caused in a number of different ways, so maybe a subset of Alzheimer鈥檚 could arise through some mechanism like this, but it鈥檚 just an intriguing possibility at this stage,鈥� he says.

One question is why beta-amyloid might accumulate in the gut in the first place. In the brain, growing evidence suggests that聽beta-amyloid plaques form to trap toxic bacteria and viruses that migrate from other parts of the body. This may explain why people with bacterial gum disease听补苍诲听herpes simplex virus聽are more likely to develop Alzheimer鈥檚 disease. Beta-amyloid may also be produced in the gut to fight toxic bacteria and viruses that enter the digestive system, but this is still speculative, says Rudd.

The team鈥檚 findings echo recent research in baboons showing that a protein called alpha-synuclein that clumps together in the brains of people with Parkinson鈥檚 disease can also聽spread from the gut to the brain. The gut is increasingly recognised as a potential starting point for a range of diseases since it is a window to the environment, says Rudd.

Proving that Alzheimer鈥檚 disease can start in the gut will be challenging, but a first step may be to measure levels of beta-amyloid in the guts of healthy middle-aged people and see how likely they are to develop the condition, says Rudd.

Vissel agrees this may be worth pursuing. 鈥淚n the Alzheimer鈥檚 field, there has been a tendency to dismiss alternative ideas,鈥� he says. 鈥淏ut we still don鈥檛 have any effective treatments, so I think it鈥檚 important to keep these other ideas alive and to properly interrogate them.鈥�

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