Text Size Normal Text Sizing Button Medium Text Sizing Button Large Text Sizing Button Text Contrast Normal Contrast Button Reverse Contrast Button Switch to Spanish Language Press Room Contact Us Sitemap Sign In Register
Link to Homepage About BrightFocus
Donate Now Get Involved  
Alzheimer's Disease Research Macular Degeneration Research National Glaucoma Research

Sign up for Email Notifications
If you would like to be notified when funding or meeting opportunities are announced please click on the link below.

Sign up for new announcements.

Please add ResearchGrants@BrightFocus.org to your institution’s white list to insure that the notification is not blocked by your organization’s SPAM filters.

This email list is not sold or distributed, and serves only as an annual reminder of the availability of research support through the BrightFocus Foundation (www.brightfocus.org). Please follow instructions on the notification emails for removal requests.

BrightFocus Research Grants Funding
Grant Funding for Alzheimer's Research
Grant Funding for Macular Degeneration Research
Grant Funding for Glaucoma Research


Alzheimer's Disease Research
Current Award

Dr. Hongmin Wang

Hongmin Wang, PhD

University of South Dakota
Vermillion, SD

Title: Using Mouse Models to Study the Role of Ubiquilin-1 in Alzheimer’s Disease
Non-Technical Title: Using Genetically Modified Mice to Study the Role of Ubiquilin-1 in Alzheimer's Disease

Duration: July 1, 2014 - June 30, 2017
Award Type: Standard
Award Amount: $250,000


A protein named ubiquilin-1 has long been considered to play a role in Alzheimer's disease. However, the exact role of the protein in Alzheimer's disease remains unclear. This research project is to investigate whether increase or depletion of the ubiquilin-1 protein in genetically modified mice changes the signs and conditions of Alzheimer's disease.


The goal of this project is to determine whether the onset and progression of Alzheimer’s disease (AD) in mice can be altered by the manipulation of a protein called ubiquilin-1. One major manifestation of AD is the accumulation of unwanted amyloid proteins in brain tissues. Previous studies conducted by these scientists have indicated that the ubiquilin-1 protein helps cell remove unwanted proteins; therefore, ubiquilin-1 may play a protective role for nerve cells affected by AD.

Dr. Wang’s group has produced genetically modified mice that either express excessive levels of ubiquilin-1 or are deficient in their expression of that protein. The scientists are currently crossing these mice with an AD mouse model, a group of mice whose specific genetic makeup allows them to serve as a model for the conditions of AD in humans. This crossbreeding will produce mice that exhibit the features of both original groups; the offspring will be AD mice that either express excessive ubiquilin-1 or lack the protein expression. Dr. Wang’s team will then investigate whether increasing or decreasing of ubiquilin-1 protein levels alters AD symptoms and progression, brain tissue structures, or the breakdown of the major AD-related proteins in the animals. The results of this study will help Dr. Wang’s team determine whether ubiquilin-1 affects the onset and progression of AD and whether the protein is a target for designing drugs to treat AD.

Investigator Biography:

Dr. Wang is an assistant professor in the Division of Basic Biomedical Sciences at the University of South Dakota Sanford School of Medicine in Vermillion, SD. He received his postdoctoral training at Johns Hopkins University School of Medicine in Baltimore, MD, and obtained his PhD from the University of Idaho in Moscow, ID. Dr. Wang’s laboratory uses genetically modified mouse models and different cell culture models, including induced pluripotent stem cells, to study AD and other disorders caused by nerve cell death in order to identify new strategies for treating such diseases.