CONTACT INFORMATIONCREDENTIALSAWARDSPUBLICATIONSRichard T. Libby, Ph.D.Contact InformationResearch LabsVisit Lab WebsiteLocationsUniversity of Rochester Medical CenterSchool of Medicine and Dentistry601 Elmwood Ave, Box 659Rochester, NY 14642Faculty AppointmentsProfessor - Department of Ophthalmology (SMD) Senior Associate Dean, Graduate Education and Post-Doctoral Affairs - Dean's Office M&D - Administration (SMD) Professor - Department of Pathology and Laboratory Medicine (SMD) - JointProfessor - Department of Biomedical Genetics (SMD) - JointProfessor - Center for Visual Science A&S (RC) - JointBiographyResearchResearch Overview Glaucoma is a complex group of diseases where many different genetic and environmental factors conspire to cause vision loss. While there are many different causes of glaucoma, the ultimate cause of vision loss in all glaucomas is the death of retinal ganglion cells (RGCs), the output neurons of the retina. Therefore, glaucoma is a neurodegeneration. Our lab focuses on the neurobiology of glaucoma. Primarily, we use mouse models of glaucoma and advanced mouse genetics to probe the pathophysiology of glaucoma. Specifically, we are interested in understanding the molecular processes that lead to RGC death in glaucoma and why are RGCs more likely to die in some patients than in others. Cell Death Pathways Active in Glaucoma To date, no molecules are known to be necessary for glaucomatous neurodegeneration nor has the initial molecular trigger(s) been identified. Identifying the molecular pathways required for RGC death in glaucoma will answer fundamental questions about neuronal pathophysiology and will identify potential therapeutic targets for the treatment of optic neuropathies. To determine the molecular degeneration cascades active in glaucoma we are taking two approaches. (1) Candidate gene analysis. The neurotrophic deprivation pathway (as one example) has been implicated as a critical pathway for glaucomatous RGC death. At both the protein and RNA level, we found that components of this pathway (e.g. BIM, JUN, and JNKs) are present in glaucomatous DBA/2J mice, suggesting that this pathway contributes to RGC death. Currently using our knowledge of the key mediator of somal apoptosis in DBA/2J glaucoma (BAX activation) and the other molecules that have been impacted in glaucoma, we are attempting to 'back track' our way up the RGC degeneration pathway. Eventually we hope this approach will lead to a complete identification of the somal and axonal degeneration pathways and to the initial molecular trigger(s) in glaucoma. (2) Genomic analysis. We are also using microarray analysis to investigate DBA/2J glaucoma. Microarray analysis has the potential to identify molecules involved in glaucomatous neurodegeneration that could not be predicted from current knowledge. In these experiments, gene expression changes at various, distinct stages of DBA/2J glaucomatous neurodegeneration are being examined. Neuronal Susceptibility Factors Elevated intraocular pressure is the best known risk factor for glaucoma. However, there is extensive patient variability in what constitutes pathogenic intraocular pressure (IOP), suggesting that other susceptibility factors are important in glaucoma. Therefore, even though glaucoma is clearly associated with IOP, susceptibility factors intrinsic to the RGCs and/or other retinal cells are likely critical mediators of glaucomatous neurodegeneration. We are attempting to define the genetic susceptibility factors that conspire with IOP to determine the probability of developing glaucoma and/or the severity of glaucoma. For instance we have shown that deficiencies in BAX gene dosage (a key molecule in the glaucomatous RGC degeneration pathway) can slow RGC loss in glaucomatous mice. These data suggest that allelic differences in components of the RGC degeneration pathway may contribute to glaucoma pathology. Also, we have been addressing the effect of blood pressure on glaucoma by backcrossing a null allele of angiotensin receptor 1 (Agtr1; deficiency in Agtr1 lowers blood pressure in mice) into DBA/2J. Low blood pressure in DBA/2J mice significantly increases the rate of glaucomatous neurodegeneration. Therefore, it appears that many diverse genetic factors can contribute to glaucomatous neurodegeneration and that the DBA/2J mouse is an effective tool in identifying these factors.CredentialsEducation1986-1990Bachelor of Science in Biology | Villanova University1997Doctorate in Biology | Boston College1998-2001Postdoctoral Scientist | 2001-2005Postdoctoral Fellow | Assistant Professor | Post-doctoral Training & Residency2001 - 2005Postdoctoral Fellow in Dr. Simon John's Laboratory. The Jackson Laboratory, Bar Harbor, ME. Neurodegeneration in Glaucoma.Awards2020The Thomas R. Lee Award for National Glaucoma ResearchSponsor: Brightfocus Foundation2020Graduate Student Society Advocacy Award2017Shaffer Prize for ResearchSponsor: Glaucoma Research Foundation2013University of Rochester School of Medicine & Dentistry Trainee Academic Mentoring Award in Basic Science.2006 - 2010Research to Prevent Blindness Career Development AwardSponsor: Research to Prevent Blindness1993 - 1997Donald J. White Teaching Excellence Award.Sponsor: Boston CollegeVIEW ALL expand_morePublicationsJournal Articles7/22/2022Marola OJ, Yablonski SER, Shrager PG, Nickells RW, Libby RT. "BclX (Bcl2l1) gene therapy lessens retinal ganglion cell soma loss but not axonal degeneration after acute axonal injury." Cell death discovery.. 2022 Jul 22; 8(1):331. Epub 2022 Jul 22. 4/16/2022Marola OJ, Howell GR, Libby RT. "Vascular derived endothelin receptor A controls endothelin-induced retinal ganglion cell death." Cell death discovery.. 2022 Apr 16; 8(1):207. Epub 2022 Apr 16. 3/16/2022Syc-Mazurek SB, Yang HS, Marola OJ, Howell GR, Libby RT. "Transcriptional control of retinal ganglion cell death after axonal injury." Cell death & disease.. 2022 Mar 16; 13(3):244. Epub 2022 Mar 16. VIEW ALL PUBLICATIONSClose WindowSchedule an appointment with Richard T. Libby, Ph.D.Please answer the following questions to help us find the right appointment for you.Important: If you believe that you have a medical or psychiatric emergency, please call 911 or go to the nearest hospital. This website is not intended for emergency care.Have you seen this provider in the last 2 years?YesNoExisting Patient Schedule or request a follow up appointment online through MyChart. If you do not have a MyChart account, please close this window and call the appointment phone number. Richard T. 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