Authors: Alice Weatherston
Amyloid-beta protein, which forms amyloid plaques within the brains of Alzheimer’s disease patients, may actually be an innate part of the immune system, a new study has revealed. The research carried out at Massachusetts General Hospital indicates that amyloid-beta may be the ‘first line of defence’ against infection in the brain, highlighting potential implications for the design of current Alzheimer’s therapies that target the protein.
Lead author of the study, Robert Moir (Massachusetts General Hospital), first proposed the idea that our view of the role of amyloid-beta in Alzheimer’s may be incomplete when he observed that amyloid-beta possesses many of the same qualities as an antimicrobial peptide. Notably, the ability to inhibit the growth of a variety of important pathogens as well as, or even better than, the antimicrobial peptide termed LL-37 utilized in the study. This preliminary study also indicated that amyloid-beta from the brains of Alzheimer’s patients was capable of suppressing the growth of cultured Candida yeast.
These initial findings by Moir have since been confirmed by other groups, leading to the current study testing the theory for the first time in living models. Moir and his team discovered that transgenic mice expressing human amyloid-beta survived longer following brain infection with Salmonella than than those without the genetic manipulation; those lacking amyloid precursor protein died even quicker.