For the past three decades, Alzheimer's disease (AD) drug discovery research has largely been guided by the amyloid hypothesis. However, more recent human genetic findings have unveiled the importance of microglia in maintaining neuronal health. These immune cells in the brain can either defend against or contribute to neurodegenerative processes. Since microglia are varied in nature, targeting them with a drug might be a double-edged sword, clearing neurotoxins while also intensifying harmful inflammation. Therefore, our research is focused on drug-like, small molecules that enhance microglial protective functions while restraining those causing neuroinflammation. Specifically, we aim to optimize inhibitors of SHIP1, a protein involved in signaling pathways and typically thought of as a brake on signaling. We hypothesize that inhibition of SHIP1 in early AD will boost microglial protective abilities, akin to releasing a brake, while simultaneously curtailing neuroinflammatory activities. This could result in a lower rate of disease progression and a decrease in cognitive decline for AD patients.