A potential new Alzheimer’s drug represses the harmful inflammatory response of the brain’s immune cells, reducing disease pathology, preserving neurons, and improving cognition in preclinical tests. Researchers have made strides in treating Alzheimer's disease by reducing amyloid-beta protein us
that implicated PU.1 as a regulator of errant microglia inflammation in a mouse model of Alzheimer’s disease. That research was a collaboration between Tsai’s lab and that of MIT computer science professor Manolis Kellis, co-led by former postdoc Andreas Pfenning, now a faculty member at Carnegie Mellon University. Ever since then, Tsai has been seeking a safe way to restore PU.1 activity to healthier levels.
They tested the effects of A11 doses on the function of human microglia-like cells cultured from patient stem cells. When they exposed the microglia-like cells to immune molecules that typically trigger inflammation, cells dosed with A11 exhibited reduced expression and secretion of inflammatory cytokines and less of the cell body shape changes associated with microglia inflammatory responses. The cells also showed less accumulation of lipid molecules, another sign of inflammatory activation.
Pharmacological tests indicated that A11 is readily cleared from tissues and is capable of reaching brain cells. Moreover, in healthy mice, the chemical successfully crossed the blood-brain barrier and remained in brain cells much longer than anywhere else. The brains of Alzheimer’s model mice treated with A11 showed more tubulin , a marker of neuronal health, than untreated controls . Credit: Image courtesy of the Tsai Lab/Picower Institute
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