Beta-amyloid Peptide, the Dr Jekyll and Mr Hyde of Alzheimer’s Disease

Beta-amyloid plaques, Aβ, is known to form insoluble aggregates in the brains of Alzheimer ’s disease (AD) patients. On the other hand, studies also found that Aβ may be an efficient means of presenting toxins to phagocytes, suggesting its potential role as anti-microbial agent. In a report published in Science Translational Medicine, Moir and colleagues went on to show more evidence (see references below for previous studies) that Aβ indeed act as an antimicrobial peptide (AMP) to protect neurons against fungal and bacterial infections. This series of experiments were done on mouse, nematode and cell culture models of AD.

The scientists generated mice overexpressing excessive amount of human Aβ, and injected the rodents’ brain with Salmonella bacteria to see whether the mice fight infection better than the wild type (WT). All the WT mice died within 96 hours, but those with human Aβ overexpression lived 30 hours longer and had fewer bacteria in their brains. In the similar experiments performed in C. elegans, Aβ-overexpression worms lived up to 3 days longer than a typical worm. More research needs to be performed in human in order to obtain a solid conclusion, as this might affect how anti-Aβ therapies should be modified in order to prevent death of AD neurons without compromising its ability to fight microbes.

arigo provides antibodies and ELISA kits for neurodegenerative diseases such as Alzheimer’s Disease.

References:

Robinson SR and Bishop GM. 2002. Neurobiol Aging 23(6): 1051-72

Wozniak MA et al. 2007. Neurosci Lett 429(2-3): 95-100

Itzhaki RF, 2014. Front Aging Neurosci 6:202

Bourgade K et al. 2015. Biogerontology 16(1): 85-98

Kumar DK et al. 2016. Science Translational Medicine 8(340)

A: Human brain tissue without blocking peptide
B: Human brain tissue with blocking peptide
C: Mouse 3T3 lysate