Alzheimer’s disease (AD) is a devastating neurodegenerative disorder that deprives more than 5 million Americans of their cognitive identities. AD cases are projected to increase as the aged population grows, at enormous personal and economic costs. AD has been defined by neuropathological hallmarks including amyloid-beta-bearing neuritic plaques, neurofibrillary tangles (NFTs), and the loss of basal forebrain cholinergic neurons (BFCN). While the underlying mechanisms contributing to early memory impairment in AD remain unclear, several prominent studies show that the degree of cognitive decline in AD patients is correlated with significant BFCN dysfunction and alterations in the physiological coding of septo-hippocampal cholinergic circuits. The primary focus of the George Lab is to understand why specific neuronal populations (such as BFCNs) are particularly vulnerable to the neuropathology commonly associated with AD. Using a combination of whole-cell patch clamp electrophysiology, RNA sequencing studies, and animal behavior we seek to understand how AD-related neuronal dysfunction disrupts the physiological processes that contribute to memory formation.