Team

Matthew Moulton, Ph.D.

Matthew Moulton, Ph.D. is an Assistant Professor in the Department of Biology at Texas A&M University. Dr. Moulton's scientific journey began in high school while participating in a research internship program in a genetics lab that sparked his desire to pursue a career in genetics research. He completed his undergraduate degree at Brigham Young University where he conducted research with Michael Whiting using DNA to reconstruct evolutionary relationships among insects, which allowed him to travel to Peru and Papua New Guinea on research trips. He then went on to complete his Ph.D. in Human Genetics at the University of Utah under the mentorship of Anthea Letsou, studying the role of glycosyltransferases in modulating signaling pathways required for embryonic development. He carried out postdoctoral research in the lab of Hugo Bellen at Baylor College of Medicine where he began his investigations into mechanisms of lipid droplet production in response to oxidative stress in neurons.

Dr. Moulton's current research focuses on understanding genetic risk for neurodegenerative disorders including Alzheimer's disease (AD). Decades of AD research has led to the identification of key molecular players in the etiology and pathogenesis of the disease. However, despite tremendous efforts, few effective therapeutic options are available for AD patients. In an effort to identify gene candidates that might prove useful for therapeutic intervention, his lab seeks to better understand the molecular underpinnings of AD. Proper lipid generation and storage is critical for healthy brain function. While it is clear that under stress conditions, neurons produce lipids that are exported and endocytosed by glia to make lipid droplets (LDs), we do not know all of the genes involved in this neuron-to-glia shuttling of lipids. His lab is undertaking an effort to identify these genes and examine their role in LD formation and clearance of the neurotoxic molecule Aβ42, a protein fragment found in the AD brain. Aβ42 is lipophilic, and preliminary data suggests that it can be taken into glial cells through the same pathway used to uptake lipids which could promote its sequestration and/or degradation. Thus, the formation of LDs not only sequesters toxic species of lipids but also may aid the elimination of Aβ42, and therefore it is an important pathway to consider for the development of AD therapies.

Dr. Moulton has broad interests in understanding molecular mechanisms of neurological disease, and his work has helped delineate the mechanistic role of lipid droplet formation in neurodegenerative disorders like Alzheimer's disease as well as a novel disease associated with variants in SREBF2, a transcription factor that regulates lipid synthesis. He is a native of Salt Lake City, Utah and enjoys spending time with his wife and four sons.

Renata Garcia

Renata Garcia is an undergraduate Biology major with a minor in Psychology and is from Monahans, Texas. She joined the lab in the fall of 2024, driven by her interest in the molecular mechanisms of neurological diseases and the genetic risk factors associated with neurodegenerative disorders. After graduation, Renata plans to attend Physician Assistant School, aspiring to become an Emergency Room Physician. In the lab, she is currently focused on assessing the effects of a deletion variant in an Alzheimer's disease risk gene. In her free time, Renata enjoys cooking, going to coffee shops, and spending quality time with friends and family.