NEW YORK: Microbes both friend and foe might contribute to the formation of amyloid plaques, according to researchers who spoke at the third annual Zilkha Symposium on Alzheimer Disease & Related Disorders, held in Los Angeles. Rudy Tanzi of Massachusetts General Hospital in Charlestown presented ongoing research on his and Robert Moir’s hypothesis that Aβ is an antimicrobial peptide, reporting that Salmonella bacteria can seed formation of plaques in the brains of mice. In turn, Sangram Sisodia of the University of Chicago focused on the bacteria that normally populate the gut. Shifting that teeming mass with intense antibiotic treatment reduced plaque burden in mice by half, he told attendees.
Making the case for a role for pathogens in AD, Tanzi noted that many of the genes recently found to be involved in Alzheimer’s disease risk function in the immune system. For example, high levels of TREM2 promote phagocytosis by microglia, while mutations in CD33 reduce phagocytosis rates, increasing amyloid plaque burden and overall Aβ load, Tanzi said.
Tanzi was the first to say his hypothesis warrants healthy skepticism. Referencing the Schopenhauer quote of the three stages of truth, whereby a novel idea is first ridiculed, then violently opposed, then finally accepted as self-evident, Tanzi placed his assertion that Aβ is an antimicrobial peptide between stages one and two. Meeting attendees were diplomatic, telling Alzforum the idea was intriguing and worthy of further investigation…..