Liqin Zhao Lab

Sugars play an integral role in building and maintaining brain infrastructure and function. Brain glucose dyshomeostasis has been indicated as a preclinical marker of Alzheimer’s disease (AD). The primary focus of our research is directed toward a molecular understanding of how sugars are dysregulated in the pathogenesis of AD. We are particularly interested in understanding how the utilization of sugars in the brain is affected by AD-linked genetic and environmental factors, leading to the development of risk phenotypes for AD. These mechanistic investigations aim to identify the key molecular targets and biomarkers for the translational development of therapeutic strategies toward AD prevention, risk reduction, and early intervention.

In summary, we are currently focused on studies in the following areas:

• Sex differences in metabolic brain aging
• ApoE2 regulation of glycolysis and brain resilience
• The role of sialic acid and sialylation in AD pathogenesis
• Impact of hyperglycemia on synaptic vesicle physiology
• Regulation of microglial homeostasis by secreted Clusterin
• Mitochondria-targeted Clusterin expression and function

The techniques used in our studies include: primary neural cell models (neurons, astrocytes, microglia), human gene stably transfected cell lines, human gene knock-in mouse models, MS proteomics, qRT-PCR arrays, gene cloning, recombinant protein production, synaptic vesicle physiology, mitochondrial biochemistry, fluorescent microscopy, behavioral modeling, and many other general methods commonly used in molecular and cellular biological, pharmacological, and drug discovery research.