Effect of Exendin-4 on Cognitive Function in Down Syndrome

Down syndrome (DS) is caused by the presence of three copies of chromosome 21, leading to dementia in later life of the patients. DS patients develop characteristic Alzheimer’s pathologies, including the amyloid-beta plaque formation, tau hyperphosphorylationto form neurofibrillary tangles and abnormal synaptic function and plasticity. Growing evidence has shown that impaired insulin signaling plays a key role in the development of AD and also the pathophysiology of DS. Exendin-4, a glucagon-like peptide-1 receptor agonist has been found to improve glucose homeostasis by promoting insulin signaling. In the current proposal, we attempt to investigate the protective effect of exendin-4 on neurons in DS and the role of insulin signaling in DS-induced cognitive deficits. This study will help us to define the mechanism underlying AD pathogenesis and the prevention and treatment of dementia in DS patients.

Faculty Supervisor:

Weihong Song

Student:

Partner:

Chongqing Medical University

Discipline:

Life Sciences

Sector:

Health and Related Sciences & Technology

University:

The University of British Columbia

Program: