Veronica Galvan, Ph.D.
Aging is, by far, the greatest risk factor for neurodegenerative diseases. Very little is known about the molecular mechanisms that connect aging to brain diseases like Alzheimer's. With the discovery of genetic pathways that can be precisely manipulated to delay the aging process, hypothesis-driven experiments can be performed to understand brain aging, and to create therapeutic strategies targeting the pathways that drive it. My research group is primarily focused on attempting to identify the molecular pathways that drive brain aging, and to determine how these processes lead to Alzheimer's disease and other neurodegenerations. Our hypothesis is that the pathways that control organismal aging can be harnessed to manipulate brain aging and thus delay or prevent brain age-associated diseases. In addition to experiments in mouse models, we routinely test potential drug candidate molecules with neurobehavioral, cellular and molecular biology tools to determine the effect of these interventions on cognitive outcomes, and to define the mechanisms involved. A second interest of my lab is to investigate the potential of modulating neurogenesis or using neuronal precursor cells for the treatment of brain injury and neurodegeneration.
Pierce A, Podlutskaya NP, Halloran JJ and Galvan V (2012) Over-expression of heat shock factor 1 phenocopies the effect of chronic inhibition of TOR by rapamycin and is sufficient to ameliorate Alzheimer's-like deficits in mice modeling the disease. J Neurochem. December 26. DOI: 10.1111/jnc.12080. View Editorial Highlight.
Lin A, Halloran JJ, Burbank RR, Korde S, Zheng W, Hussong S, Podlutskaya N, Strong R, Richardson A, Fox PT, Lechleiter J, Hart MJ, Galvan V (2012) Chronic rapamycin restores brain vascular integrity through eNOS activation and improves memory in mice modeling Alzheimer’s disease. J Cereb Blood Flow and Metab. In review.