Gregorio Valdez, PhD
Assistant Professor, Virginia Tech Carilion Research Institute
Assistant Professor, Biological Sciences, College of Science, Virginia Tech
Assistant Professor of Internal Medicine, Virginia Tech Carilion School of Medicine
The Valdez Laboratory is interested in discovering molecules that protect synapses from the ravages of aging and age-related neurological diseases. Synapses are the sites where information is received and transmitted throughout the central nervous system and between motor neurons and muscles. They are also a primary site of entry for growth factors and other molecules that neurons and muscles need to properly function and survive. Unfortunately, aging and a variety of diseases cause this critical bridge of communication and port of entry to fall apart, resulting in the erosion of cognitive and motor skills. Because of this, Valdez and his team are invested in discovering and manipulating molecules that function to prevent the destruction of synapses. In much of the laboratory's work, the researchers study the motor neuron and muscle synapse, the neuromuscular junction. This is a large and readily accessible synapse that is significantly affected by normal aging and the progression of diseases, including amyotrophic lateral sclerosis. Using mouse models of injury, disease, and normal development and aging, the scientists seek to identify new molecules and signaling pathways that serve to protect or maintain healthy synapses. Valdez and his team utilize a number of molecular and imaging techniques, including chronic in vivo imaging, genetic manipulations, and viral-based vectors. The hope is that some of these molecules, in addition to maintaining the neuromuscular junction, will dually function to maintain the proper functioning of brain synapses.
For a more complete listing of Gregorio Valdez's publications, visit PubMed.
Education and Training
- Harvard University: Postdoctoral fellowship, Molecular and Cellular Biology
- Stony Brook University: PhD, Neurobiology and Behavior
- Lehman College/CUNY: BS, Biochemistry
- Harvard University
Senior Postdoctoral Fellow, Department of Molecular and Cellular Biology
Awards and Honors
- Distinguished Honoree, March of Dimes, 2015
- Finalist, Earl Stadtman Investigators Search, National Institutes of Health, 2011-2012
- Ruth L. Kirschstein National Research Service Awards, National Institutes of Health, 2007-2010
- Carl Storm URM Fellowship, Gordon Research Conference, 2006
- Minority Biomedical Research Support, National Institutes of Health, 1993-1996
- Vaughan SK, Kemp Z, Hatzipetros T, Vieira F, Valdez G. (2015). Degeneration of proprioceptive sensory nerve endings in mice harboring amyotrophic lateral sclerosis-causing mutations. Journal of Comparative Neurology 523(17), 2477-94.
- Dittmar WJ, McIver L, Michalak P, Garner HR, Valdez G. (2014). EvoCor: a platform for predicting functionally related genes using phylogenetic and expression profiles. Nucleic Acid Research.
- Valdez G, Hayer MP, Feng G, Sanes JR. (2014). The role of muscle microRNAs in repairing the neuromuscular junction. PLOS ONE.
- Samuel MA, Valdez G, Tapia JC, Lichtman JW, Sanes JR. (2012). Agrin and synaptic laminin are required to maintain adult neuromuscular junctions. PLoS One 7(10), e46663.
- Valdez G, Tapia JC, Lichtman JW, Fox MA, Sanes JR. (2012). Shared resistance to aging and ALS in neuromuscular junctions of specific muscles. PLoS One 7(4), e34640.
- Valdez G, Tapia JC, Kang H, Clemenson GD Jr, Gage FH, Lichtman JW, Sanes JR. (2010). Attenuation of age related changes in mouse neuromuscular synapses by caloric restriction and exercise. Proc Natl Acad Sci USA 107, 14863–68.
- Williams AH*, Valdez G*, Moresi V, Qi X, McAnally J, Elliott JL, Bassel-Duby R, Sanes JR, Olson E. (2009). MicroRNA-206 delays ALS progression and promotes regeneration of neuromuscular synapses in mice. Science 326, 1549–54.
- Nishimune H, Valdez G, Miner JH, Sanes JR. (2008). Laminins promote postsynaptic maturation by an autocrine mechanism at the neuromuscular junction. J Cell Biol 182, 1201-15.