Neurofibrilliary tangles in the hippocampus of an aging person with Alzheimer’s pathologyWIKIMEDIA, PATHOThe tangled buildup of tau protein in brain cells is a hallmark of the cognitive decline linked with Alzheimer’s disease. Antibodies have been shown to block tau’s spread, but some scientists worry it could also fuel inflammation. Now, researchers from Genentech in San Francisco and colleagues have found that an antibody’s ability to recruit immune cells—known as its effector function—is not necessary for stopping tau’s spread, the team reported today (July 28) in Cell Reports.
“Our results suggest that, given that effector function is not required for efficacy [in treating tau accumulation], going without it could offer a safer approach for immunotherapy,” study coauthor Gai Ayalon of Genentech told The Scientist.
Alzheimer’s disease causes a characteristic constellation of pathologies: accumulation of amyloid-β plaques outside neurons, neurofibrillary tangles of tau inside brain cells, and chronic inflammation. Clinical research has mostly focused on targeting amyloid-β with antibody therapies, and several treatments based on this approach are currently in clinical trials.
But recent efforts have zeroed in on tau as a new potential target. Antibodies are known to spur the brain’s defense system, microglia, to absorb and degrade tau, but their recruitment of immune cells may also worsen inflammation. Ayalon and colleagues wondered ...
