Alzheimer’s disease is the most common cause of dementia, manifested as memory loss and other cognitive impairments that interfere with daily life. Converging evidence supports the notion that Alzheimer’s disease is the result of selective vulnerability of specific neural networks. Yet, our molecular understanding of selectively vulnerable neural networks is very limited. Only by understanding the molecular phenotype of these cellular networks can we devise strategies to protect these networks from degeneration. In collaboration with Dr. Edward Lee, we are studying cellular transcriptomic variations from human brains with the hope of providing a detailed molecular phenotype of vulnerable cellular networks as a foundation for developing therapeutic strategies for Alzheimer’s disease.