ALZHEIMER’S Disease is the most common form of dementia, affecting an estimated 30 million people worldwide. The cause of the condition is unknown, but the prime suspect is amyloid-beta (Aβ), a 42-amino acid peptide which accumulates within neurons to form insoluble structures called senile plaques that are thought to be toxic. Aβ is synthesized in all neurons; it is associated with the cell membrane, and is thought to be involved in cell-to-cell signalling, but its exact role has eluded researchers.
A new study published in the open access journal PLoS One now shows that Aβ is a potent antibiotic that can prevent the growth of a number of disease-causing microbes. The study provides the first evidence of a normal role for Aβ, and also raises the intriguing possibility that Alzheimer’s Disease occurs as a result of the immune system’s response to infection. The findings could make researchers re-think Alzheimer’s, and have implications for how the condition is treated.