Gregorio Valdez, PhD
Assistant Professor, VTC Research Institute
Assistant Professor, Biological Sciences, College of Science at Virginia Tech
Research Program Summary
My lab 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, my lab is invested in discovering and manipulating molecules that function to prevent the destruction of synapses. In much of our work, we 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, we seek to identify new molecules and signaling pathways that serve to protect or maintain healthy synapses. My lab utilizes a number of molecular and imaging techniques, including chronic in vivo imaging, genetic manipulations, and viral-based vectors. Our 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.
Education and Training
- Harvard University: Postdoctoral fellowship, Molecular and Cellular Biology
- Stony Brook University: Ph.D., Neurobiology and Behavior
- Lehman College/CUNY: B.S., Biochemistry
- Harvard University
Senior Postdoctoral Fellow, Department of Molecular and Cellular Biology
Awards and Honors
Dr. Valdez received a Ruth L. Kirschstein National Research Service Award from the National Institute of Neurological Disorders and Stroke/National Institutes of Health to examine the molecular basis of age-related synaptic alterations as a postdoctoral fellow from 2007 to 2010.
- 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.