Fang Du

Assistant Research Professor
Primary office:
785-864-6373
Smissman Research Laboratories
Room B62


Summary

Fang Du M.D., Ph.D., received his doctorate in neuroscience and neurodegenerative diseases from the Chinese University of Hong Kong.  He completed his first postdoctoral training in neurodevelopmental disorder at the State University of New York, Stony Brook.  In 2013, he joined Dr. Shi Du Yan’s research group in the Smissman Research Laboratories at the University of Kansas as a postdoctoral researcher, and was promoted to Assistant Research Professor in 2018.

The main goal of Dr. Du’s research is to understand the pathogenesis and explore new therapeutic strategies for treatment of neurodegenerative disorders such as Alzheimer's disease (AD) and Parkinson’s disease (PD).  Mitochondrial dysfunction and synaptic dysfunctions are early pathological features of AD-affected brains.  He first revealed that decreased PTEN-induced putative kinase 1 (PINK1) expression is associated with AD pathology, and gene therapy-mediated neuronal PINK1 promotes the clearance of damaged mitochondria by augmenting autophagy signaling, thus rescues amyloid-associated pathology, oxidative stress, as well as mitochondrial and synaptic dysfunction.  He also demonstrated that increased expression of active presequence protease (PreP, a specific mitochondrial peptidasome) in neurons significantly enhances degradation of Aβ, attenuates AD-like mitochondrial amyloid pathology.

Another strategy he employed to investigate the role of dysfunctional mitochondria in AD pathogenesis is the Cytoplasmic hybrid (Cybrid) technology, with the transfer of mitochondria from AD-affected patients to mitochondrial-depleted cell lines (Rho0 cells).  AD Cybrid cells, when induced to differentiate, developed stunted projections.  Mitochondrial transport and functions within neuronal axons were impaired in AD-derived mitochondria, while antioxidants reversed these deficits in axonal mitochondria.  Dr. Du further disclosed the increased reactive oxygen species levels, induced by mitochondrial dysfunction, were activated through p38 MAPK pathway, and finally contributed to synaptic maldevelopment in differentiated AD Cybrids.

Using the induced pluripotent stem (iPS) cell technology, he elucidated the importance of mitochondrial bioenergetics in human dopaminergic neuronal differentiation.  He further revealed the significance of astroglia in maintaining mitochondrial functions during dopaminergic neuronal differentiation.  His study on the glial-neuronal interaction model provides an approach for therapeutic discovery for PD.

Dr. Du’s research has been continually supported by NIH and foundation grants. In 2018, he was awarded Alzheimer’s Association International Research Grant (AARG). He has published articles in peer-review journals, including Brain, The Journal of Neuroscience, Human Molecular Genetics, Stem Cell Reports, Glia, Molecular Neurobiology, Journal of Alzheimer’s Disease, Free Radical Biology and Medicine, Scientific Reports, Nature Communications, Hepatology, Diabetes, etc.  His studies were highlighted in 'Nature Reviews Neuroscience' and reported by several news outlets, and his publications has been selected as an Editor's Choice articles of ‘BRAIN’ and ‘Journal of Alzheimer’s disease’. He is a member for American Society of Neuroscience (SfN) and American Association for the Advancement of Science (AAAS).


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