Research in the Zheng Laboratory focuses on Alzheimer's disease (AD), the most common form of neurodegenerative disease, and two pathological hallmarks of AD, beta-amyloid plaques and neurofibrillary tangles. These two physiological hallmarks of AD are formed by A-beta peptides derived from the amyloid precursor protein (APP), and an aggregation of a hyperphosphorylated protein, Tau, respectively. Mutations in APP and the presenilin family of proteins lead to dominant inheritance of familial AD, establishing a central role of APP and presenilins in AD pathogenesis. The Zheng Laboratory is interested in understanding the pathophysiological functions of APP and presenilins, deciphering the interactions of amyloid and neurofibrillary tangle pathology, and identifying novel therapeutic strategies that target amyloid plaques or neurofibrillary tangles. To achieve these goals, the Zheng lab works in mouse models of Alzheimer's Disease, and complements the study of mouse genetics with molecular, neuroanatomical, electrophysiological and behavioral approaches.