Alzheimer's disease currently has no effective treatments or means to preserve cognitive function. Here, we are targeting a calcium channel known to be dysregulated early in the disease process and contributes to a host of AD-associated symptoms and memory loss. By restoring normal function of this channel, we can reduce the histopathological features of amyloid and tau aggregation, preserve normal synaptic structure and function, and prevent the memory impairments that characterize this disease. We are approaching this drug discovery project in a novel fashion, in the hopes that a new approach will provide greater disease modifying and preventative outcomes than previous strategies based on later-stage histological targets.