Xudong Huang, PhD

Dyshomeostasis of cerebral biometals (Fe, Cu, Zn) and oxidative stress are neurochemical processes that contribute to the development and exacerbation of Aβ amyloid pathology that is characteristic of Alzheimer's disease (AD). Therefore, the main thrust of Dr. Huang's laboratory is to study the roles of metallomics and oxidative stress in AD and other human diseases, design and characterize novel compounds for Alzheimer's therapeutics and diagnosis. We also focus upon unraveling the chemical mechanisms of the redox activity of Aβ and homocysteine in relation to the pathophysiology of AD. Our studies center upon in vivo analyses, using an established transgenic mouse model of AD. Determination of in vivo biochemical roles of biometal dyshomeostasis and oxidative stress in AD pathology will provide a firm scientific base for understanding the potential of amyloid-specific metal chelation and antioxidant therapies for AD. Dr. Huang's previous training and current research focus will allow for the discernment of whether precise oxidative processes operate as a function of shared disease processes, aging alone, or instead are selective for AD pathogenesis.