About the Zheng Lab

Staining of Mouse APP Knock-in (320x240)
credit: Hui Zheng LabAmyloid plaques (red) and reactive gliosis (green) visible in staining of APP-knock-in mouse model

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.

Current Projects Include:

Tau and TFEB staining (320x240)
credit: Hui ZhengTau transgenic mice treated with TFEB display clearing of Neurofibrillary Tangles (red), when compared to mice untreated with TFEB

Understanding the mechanisms of APP in synaptic function and dysfunction using mouse mutants with tissue-specific deletion of APP or by expressing different APP domains;

Deciphering the pathogenic processes downstream of A-Beta, NFTs or both combined by studying mouse models with either plaques, tangles or both;

Investigating the role of astroglia and neuron-glia signaling in AD pathogenesis;

Developing tau/NFT-based therapies by targeting intracellular autophagy and lysosomal degradation pathways.