Photo of Xiangyou  Hu, Ph.D.

Xiangyou Hu, Ph.D.

Assistant Professor, Neuroscience
Academic Office Location:
UConn Health
263 Farmington Avenue
Farmington, CT 06030-3401
B.S.Anhui Medical UniversityMedicine
M.S.Department of Anatomy, Henan Medical UniversityNeurobiology
Ph.D.Department of Neurobiology, School of Life Sciences, University of Science and Technology of ChinaNeurobiology

Post-Graduate Training
PostdoctoralCleveland Clinic Lerner Research InstitutePostdoctoral Research Fellow, Department of Neurosciences

Name of Award/HonorAwarding Organization
William E. Lower Award for Basic Science ResearchCleveland Clinic Lerner Research Institute
Innovator Award for identification of RTN3 aggregates in Alzheimer’s brainsCleveland Clinic
Name & DescriptionCategoryRoleTypeScopeStart YearEnd Year
Alzheimer's Association International SocietyProfessional/Scientific OrganizationMemberExternalInternational2020
Society for NeuroscienceProfessional/Scientific OrganizationMemberExternalNational2015

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: Summer 2023, Fall 2023, and Spring 2024


Journal Articles


Title or AbstractTypeSponsor/EventDate/YearLocation
BACE1 deletion in the adult reverses epileptiform activity and sleep-wake disturbances in AD mice modelsTalkUConn Health Department of Neuroscience2022UConn Health
Deletion of neuronal BACE1 causes mice memory deficits.TalkAlzheimer’s Association International Conference2020Amsterdam, Netherlands
BACE1 deletion in the adult mouse reverses preformed amyloid deposition and improves cognitive functions.TalkUniversity of Science and Technology of Chin2019China
Accumulation of lysosomal vesicles and ferritin in dystrophic neurites and their selective degradation in Alzheimer’s disease mice brain.TalkSociety for Neuroscience Annual Meeting2019Chicago, IL
BACE1 regulates Schwann cell proliferation in the sciatic nerve.TalkAnhui Medical University2018China
BACE1 deletion removing pre-formed amyloid plaques in 5xFAD mice.TalkUConn Health Department of Neuroscience2018Farmington, CT
Exploring BACE1 physiological function in BACE1-null mice.TalkUniversity of Science and Technology of China School of Life Sciences2016China
BACE1 regulates hippocampal astrogenesis via the Jagged1-Notch pathway.TalkAnhui Medical University2015China
Schwann cell BACE1 is required for remyelination of peripheral nerves.TalkInternational Conference on Alzheimer's and Parkinson's Diseases2015Nice, France