Groundbreaking research reveals lithium deficiency in human and mouse brains as a contributing factor to the onset and progression of Alzheimer’s disease. Amyloid plaque binding reduces lithium bioavailability, accelerating neurodegeneration. Novel amyloid-evading lithium compounds reverse pathology and restore memory in murine models. Parallel studies demonstrate successful replacement of diseased microglia with allogeneic donor cells, significantly slowing symptoms in genetic neurodegenerative diseases like Tay-Sachs and Sandhoff, offering potential new therapeutic avenues.