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We will test the novel concept that specific chemical modification drives unusual targeting of Alzheimer’s-linked “tau” proteins to the dendritic spines of neurons. This targeting might provide a mechanistic link between amyloid and tauopathies, hallmarks of the Alzheimer’s disease (AD) process. Therefore, the successful completion of this project will provide a more complete mechanistic model for AD than available at present.

A national consensus panel was convened with support from the BrightFocus Foundation to review and summarize the need to move toward home-based dementia care as a critical component of care services for people with Alzheimer's disease and related dementias (AD) in the coming decades. Panel findings show the evidence for providing wholistic, individualized home-based dementia care for patient and caregivers benefits is robust and growing. However to support this shift in care delivery to home settings, several challenges must be tackled, including to improve research methods to better disseminate evidence into practice; improve opportunities for home-care financing; train an expanded dementia care workforce; and take advantage of technology applications for the home. The findings are being disseminated internationally to policy makers, clinicians, researchers, and aging services providers. In addition, they were presented at the Alzheimer’s Association International Conference in 2016 and are a pre-summit activity to inform the Advisory Counsel of the National Alzheimer Project Act (NAPA) plans for a Fall 2017 Research Summit on Care and Services for Persons with Dementia and their Caregivers.

We have identified a unified signaling pathway based on activation of innate immune system which results in an inflammatory cascade resulting in POAG. We have identified that cell trauma causes low-molecular-weight hyaluronic acid to start the pathway. Prevention of degradation of high-molecular-weight hyaluronic acid by potent hyaluronidase inhibitor could be novel therapy and the first therapy directly aimed at the cause of POAG.

Alzheimer’s disease (AD) destroys brain cells, causing memory loss and problems with thinking and behavior severe enough to affect work, lifelong hobbies, and social life. New neurons are born in the adult brain (called “adult neurogenesis") and this process is impaired in AD, suggesting that impaired cognitive function in AD might, at least, in part, be due to impaired neurogenesis in the adult brain. ADAM10 is a protein that plays an important role in AD, as it prevents the generation of a toxic protein that causes AD. Dr. Choi’s team hypothesizes that ADAM10 also plays critical roles in adult neurogenesis, and they propose various animal and cell culture experiments to validate their hypothesis.

This project uses viral gene therapy in mice to repair genetic defects that lead to AMD like pathology.

This project aims to develop advanced imaging methods to understand the spatial organization of different cell types in the brain and their vulnerability to tau propagation in Alzheimer’s disease.