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Eric Daniel Hamlett PhD

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  • Assistant Professor
  • College of Medicine
  • Pathology and Laboratory Medicine
Academic Focus
  • Down Syndrome/Alzheimer's Disease
  • Healthy Brian Aging
  • Neuroscience
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I have 18 years of research experience and was appointed as an Assistant Professor (July 2019) in the Department of Pathology and Laboratory Medicine at the Medical University of South Carolina (MUSC). My research focuses on early drivers that precede pathological responses in the brain (like Alzheimer’s disease). My lab is seeking to use convergent approaches to better understand the lipoxygenase system specifically in the brain. The omega-x fatty acid (FA) inputs to this systems have been steadily leaning toward increased omega-6 resulting in decreases in omega-3 FA. A deficiency of DHA is associated with several neurological diseases, including Alzheimer’s disease (AD), schizophrenia, Parkinson’s disease, and major depressive disorders. The magnitude of the decrease in the omega-6/omega-3 FA ratio is not uniform in all brain areas and is most significant in the cortex, striatum and hippocampus. This pattern of input deficiency grows with age and is thought to create imbalances in lipoxygenase-mediated output lipid metabolites that convey important bioactive properties in the brain.

The dominant lipoxygenases (LOX) in the brain ( 5, 12 and 15 LOX) work together to process omega-6/omega-3 FAs into a wide range of output lipid metabolites. Some LOX-mediated lipid metabolites are inflammatory. LOX metabolize omega-6 fatty acids into arachidonic acid and then further into leukotrienes and prostaglandins. The leukotrienes are potent inflammatory lipid mediators and were found to be elevated with age and in individuals with AD. Prostaglandins control processes such as inflammation, blood flow, the formation of blood clots and are involved in responses to injury and illness. Most prostaglandins showed significant increases in the aging heart and some prostaglandins cause severe dysfunction in glial cells when elevated. Together, elevations in leukotrienes and prostaglandins support that lipoxygenase processing of omega-6 FA is elevated with increasing age. Other LOX-mediated lipid metabolites are neuroprotective. Brain lipoxygenases metabolize omega-3 fatty acids into a set of specialized pro-resolving mediators (SPMs), a family of G protein-coupled receptors and signaling effectors that regulate tissue homeostasis and robustly modulate inflammation. In the clinic, decreased SPM levels have been correlated with age and further support that a deficiency in omega-3 FA input to lipoxygenase exists. In 2020, we published promising studies on administration of proresolution mediators to a mouse model of chronic inflammation. We discovered that resolution enhancement could significantly reduce microglial activation and peripheral cytokine expression in a mouse model suffering from neurodegenerative paradigms.

Clinical measurements of brain omega-x FAs and lipoxygenase output lipid metabolites are not currently possible. To overcome this barrier, we are building new technologies to explore brain lipoxygenase input/output in the brain. We utilize extracellular vesicles (EVs) produced from the cells in the brain directly from clinical blood samples. EVs carry representative FA and lipid snap-shots from the host cells from which they were derived. Since brain EVs readily cross the blood-brain barrier, approximately 8% of total blood EVs are neuronal in origin. This unique approach will enables direct quantification of omega-6/omega-3 FAs, leukotrienes, prostaglandins and SPM directly from neurons. The method is rigorous and can be adapted to astrocytes, microglial and oligodendrocytes, allowing cell-specific profiling of input/output molecules to the lipoxygenase system in the brain. The technology is also versatile and our lab welcomes collaboration with others to probe literal snapshots of brain cells using only clinical blood samples.

Click the Research Profile above to learn more exciting research happening in my lab.