Kiminobu Sugaya
University of Central Florida, USA
Title: Small molecule based neuroregeneration therapy for Alzheimer's disease
Biography:
Kiminobu Sugaya has been a professor of medicine at the Burnett School of Biomedical Science, College of Medicine, University of Central Florida since 2004. He is Director of the Multidisciplinary Neuroscience Alliance, and a Chair of the Central Florida Chapter of the Society for Neuroscience. His primary research focus has been developing regenerative medicines for neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease using iPS and adult stem cells. Dr. Sugaya earned his B.S., M.S. and Ph.D. from the Science University of Tokyo. He received postdoctoral training under the direction of Dr. Ezio Giacobini, who is responsible for breakthroughs in cholinesterase Alzheimer's disease therapies.
Abstract:
Despite decades of investigations in both laboratory and clinic, the pathophysiological mechanism of Alzheimer’s disease (AD) still remains unknown. Current problem of developing AD research is that many treatments have been found to be very effective in AD animal models but they failed show significant effects in clinical trials. Thus, establishment of an effective treatment in a model, which represent pathophysiology of AD is needed. Previously, we were able to show improved cognitive function of aged, memory-impaired animals through the implantation of human neural stem cells (NSCs), which produced much excitement throughout the research world and the overall medical community; given the implication that this could lead to a cure for all neurodegenerative diseases, including AD. However, when we transplant NSCs to a transgenic animal model produces Amyloid-β (Aβ) plaque formation in the brain by expressing familial AD mutant amyloid precursor protein (APP), mimicking the pathological condition of AD, we did not find any new neuronal development formed from the donor cells. This indicates that transplantation of NSCs by itself may not be a cure for AD. Here we show that the combination drug therapy of Posiphen (reducing APP level) and NBI-18 (increasing endogenous neural stem cell) increased neurogenesis and significantly improved memory in the transgenic AD mouse model. This combination therapy could bring us an effective treatment for AD. I will further discuss the use of iPS cell to confirm this efficacy in vitro 3D human AD brain model.