Dr. Xinkun Wang

Xinkun Wang, Ph.D.
Associate Research Professor

Office: 139 PCL
Voice: (785) 864-4589

Research Summary

Dr. Xinkun Wang’s research interest is in neurogenomics, i.e., the use of genomics approaches to study the brain. The long-term goal of his research is to reveal genome changes during brain aging and the genomic basis of aging-associated neurodegenerative diseases, including Alzheimer's disease. Currently, the focus of his research is to unravel the underlying mechanisms for the degeneration of neurons that are particularly vulnerable to the aging and disease process. Examples of these vulnerable neurons are those in the layer II of the entorhinal cortex and the CA1 region of the hippocampus, both of which are among the earliest impacted neurons in Alzheimer's disease.

As in other types of cells in our body, the genomic DNA in brain neurons undergoes systematic changes during the aging process. However, the extent and nature of these changes are still largely unknown. It has been shown that aging-associated genomic changes are brain region specific. A brain region’s neuronal genomic profile determines, to a large degree, how it behaves in aging and responds to neurodegenerative conditions. By studying regional genomic profiles in the mammalian brain, followed by neurobiological measurements, Dr. Wang finds that oxidative stress, glutamate excitotoxicity, and mitochondrial dysfunction play an important role in selective neuronal degeneration. Furthermore, he finds that genome instability is another underlying factor for selective neuronal vulnerability and loss.

The ultimate goal of studying neuronal vulnerability in aging-associated neurodegenerative diseases is to develop intervention strategies to protect vulnerable neurons. Toward this goal, Dr. Wang’s future work includes developing therapeutic agents in collaboration with medicinal chemists to increase the viability of vulnerable neurons. Improving genome stability of vulnerable neurons will be used as the main entry point in this front.

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