Alzheimer’s disease (AD), the most common cause of age-related dementia, is a debilitating neurodegenerative disease that leads to progressive memory loss, cognitive impairment, and ultimately death. The β-site APP cleaving enzyme 1 (BACE1) is a major drug target for AD treatment because BACE1-mediated cleavage of APP is the first step in the generation of pathogenic amyloid-β peptides. My lab focuses on investigation of BACE1 biological functions and the roles of BACE1 in the pathogenesis of Alzheimer’s disease using both conditional and constitutional BACE1 knockout mice.

Considering the fact of epileptiform activity and sleep disorders occurs more frequently in AD patients, our one project is examining whether BACE1 inhibition impacts seizure activity and sleep disorders in AD mice and further characterize the correlation of plaque loading with epileptiform spikes, NREM and REM sleep times in AD mice models.

 Lower urinary tract dysfunction (LUTD) is another most common symptoms in AD. However, the pathophysiological link between AD and LUTD is not well defined. We have another project focusing on investigation of bladder pathology, nerve innervation, neurotransmitters and the receptors distribution, and muscle-specific responses in AD bladders.  

Accepting Lab Rotation Students: Fall Block 2024, Spring 1 and 2 Block 2025

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