Dr. Eric D. Hamlett is an Assistant Professor in the Department of Pathology and Laboratory Medicine and the Research Coordinator of the MUSC Carroll A. Campbell, Jr. Neuropathology Laboratory program, which is funded in part by the NIH, NCI, the Down Syndrome International Biobank Program. the Children’s Tumor Foundation, and through various charitable gifts.
Dr. Hamlett is focused on understanding the mechanisms underlying the pathogenesis of Alzheimer's disease (AD), on finding novel therapeutic targets, and on promoting healthy aging. Dr. Hamlett serves as an Associate Editor for the Journal of Frontiers in Neuroscience and has served as a repeat reviewer for several journals. He comes from a socioeconomic background that is underrepresented in science and stem fields and is a proponent of maximize inclusiveness of a variety of underrepresented talent in Science and Research. Dr. Hamlett seeks to enhance educational opportunities for all students, especially for those that had fewer training opportunities and/or disadvantageous struggles.
Dr. Hamlett received his B.S. degree in biology and chemistry from Western Carolina University in 2002. He was a Scientist in the McAllister Heart Institute and later served as the Manager of the UNC Systems Proteomics Research Center. He then attended the Medical University of South Carolina, receiving his Ph.D. in Neurosciences in 2017. Dr. Hamlett’s postdoctoral research was performed at the University Denver Knoebel Institute for Healthy Aging (2017-2018). Prior to his arrival at MUSC, Dr. Hamlett served on the communications team for the T21 research society and won several competitive awards in research innovation and entrepreneurial startup.
The Hamlett laboratory is focused on determining what molecular abnormalities are responsible for the development of neurodegenerative responses associated with AD and using this information to develop effective new treatments to slow or stop this progressive disease. His lab has found evidence that abnormal shedding of AD pathogenic molecules occurs decades, before the first cognitive symptoms are of AD, are experienced. Based on this evidence, we have developed a novel experimental pipeline in which inappropriate passage of pathogenic molecules results in the development of several aspects of the disease in mice. In contrast to previously developed AD mouse models, this system allows normal mice to readily develop several neuropathological signatures of AD at a very high frequency. This model thus gives us a unique opportunity to establish how pathogenic shedding can drive the development of AD without the introduction of major genetic changes and without promoting extremely aggressive disease phenoytpes at young age. Using this model, his lab aims to identify novel classes of compounds that effectively inhibit the pathogenic spread of AD in vivo.
To identify additional therapeutic targets in AD, the Hamlet lab is also using NextGen sequencing methods to comprehensively identify genetic and epigenetic abnormalities that are specific to glial cells during different stages of AD progression. These studies are being performed using brain specimens collected from human donors to the Carroll A. Campbell, Jr. Neuropathology Laboratory and in our mouse models of AD. These comprehensive approaches thus continue to identify potential new treatment targets, thereby laying the groundwork for the development of effective new therapies for AD.