Targeting of impaired antimicrobial immunity in the brain for the treatment of AD

The Publication

Alzheimer’s Disease (AD) is the most common neurodegenerative disease that leads to clinical dementia. The cause remains unknown, despite a massive amount of research. To date, the most commonly accepted hypothesis is the amyloid cascade, with the idea that the deposition of amyloid-beta plaques triggers neurodegeneration. However, all clinical trials that have targeted the deposition of plaques has failed, suggesting we need a better understanding of the treatable factors of the disease for new treatment targets. Notably, an alternative explanation lies with the infection hypothesis, and the potential role of antimicrobial defences.

The present article explored the notion that low-grade infection leads to the deposit of plaques, which have antimicrobial activity, and precedes the development of AD. However, the infection, albeit chronic, can lie silent for decades because of an efficient antimicrobial immune response in the brain. However, a chronic inflammatory state is induced which eventually results in neurodegeneration.

That changes in the brain’s antimicrobial immune response occurs during ageing, particularly in those with Alzheimer’s, is a concept that should be utilised to target interventions to prevent or limit the progression of AD. Whilst it is clear that AD cannot be linked to a specific microbe, if we can link subgroups of AD individuals to chronic infections, then there is the potential to treat preclinical AD, stopping progression.

Our Response

There has been much media surrounding microbes in immunity, however the antimicrobial community which mediates immunity in the brain, remains complex. At Think Though Nutrition we are interested in how nutrition and lifestyle could influence this microbial community to prevent the progression of a polymicrobial induced inflammatory disease state.