Gut bacteria play a key role in Alzheimer’s and dementia


Amyloid plaques are sticky proteins that build up in the brains of Alzheimer’s patients. This prompts an immune response, which causes chronic inflammation and in turn this damages the nervous tissue.


Andreas Bäumler and his team at UC Davis School of Medicine showed that if they injected mice with E coli and Salmonella bacteria, curli fibril proteins (CsgA) produced by the bacteria stuck to other curli fibres and to the gut wall, forming colonies resembling plaques. This caused an immune response.


These aggregates of curli fibrils are similar in structure to the amyloid fibrils in the brain plaques. Bäumler hypothesized that what was happening was a case of ‘mistaken identity’ by the immune system, which attacked the colonies in the gut and the plaque in the brain.


The research team then showed that when they destroyed the ability of the proteins in the gut to aggregate, the inflammation in the brain and the immune reaction stopped.


“The CsgA peptide and beta-amyloid don’t have anything genetically in common. The similarity is only in the structure of the amyloids they form. Our study indicates that there is some structural feature of amyloids that triggers the innate immune system,” Bäumler said.


Chris Woollams, former Oxford University Biochemist added, “Studies like this are crucial to understanding the process in Alzheimer’s. Hitherto drug companies have been unsuccessful because they were just shooting in the dark. More work on the gut may even show the solution to Alzheimer’s lies in healing your gut, rather than tackling problems directly in the brain”.


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