Xianlin Han, PhD

Personal Statement:

Laboratory studies the role of lipid metabolism in age-related diseases with a major focus on Alzheimer’s disease. Previous work has revealed that among the earliest Alzheimer’s-related lipid alterations is a dramatic deficiency in a class of myelin-specific lipids, known as sulfatide, that is modulated in an age- and apolipoprotein E (apoE) isoform-dependent fashion. Research findings strongly support the notion that sulfatide plays a critical role in apoE-mediated Ab metabolism and Alzheimer’s pathogenesis. Current research efforts focus on elucidating the underlying molecular mechanism(s) leading to sulfatide deficiency at the earliest stages of Alzheimer’s, identifying and describing the consequences of severe sulfatide losses (e.g., Ab deposition, tau hyperphosphorylation, astrocyte activation and ventricular enlargement) and the mechanisms leading to these sequelae and determining the connections between sulfatide deficiency and other Alzheimer’s risk factors (including aging and diabetes). Numerous animal models (e.g., sulfatide conditional knockout mice, AD mouse models, human apoE knockin mice and diabetic animal models) are used to study the role of sulfatide in aging and Alzheimer’s development.