He exposed the mouse hippocampus to the most toxic component of β-amyloid plaques, known as the Aβ peptide, and found that long-term potentiation was impaired before any neurons had died or plaques had formed. In addition, animal models of early Alzheimer’s disease displayed memory deficits before any detectable accumulation of plaque or evidence of cell death. While examining gene expression in hippocampal cells exposed to the Aβ peptide, Shelanski discovered that the peptide
