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Richard T. Libby, Ph.D.

Contact Information

Phone Numbers

Appointment: (585) 276-3000

Biography

Research

Research 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.

Credentials

Faculty Appointments

Education

1997
Doctorate in Biology | Boston College

2001-2005
Postdoctoral Fellow |

1998-2001
Postdoctoral Scientist |

1986-1990
Bachelor of Science in Biology | Villanova University

2006-0
Assistant Professor |

Awards

2017
Shaffer Prize for Research
Sponsor: Glaucoma Research Foundation

2013
University of Rochester School of Medicine & Dentistry Trainee Academic Mentoring Award in Basic Science.

2006 - 2010
Research to Prevent Blindness Career Development Award.

2005
David Bryant Trust. Unlocking Mechanisms Behind Vision Loss in Glaucoma.

2004
Lewis Rudin Glaucoma Prize. Awarded by The New York Academy of Medicine for the "most outstanding article on glaucoma published during the previous year". First author of article.

1993 - 1997
Donald J. White Teaching Excellence Award. Awarded four times for my work as a teaching assistant in the lecture course, Introduction to Biology, Boston College. 1993,1995,1996,1997

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Publications

Journal Articles

12/6/2016
Majumder S, Zhu G, Xu X, Senchanthisai S, Jiang D, Liu H, Xue C, Wang X, Coia H, Cui Z, Smolock EM, Libby RT, Berk BC, Pang J. "G-Protein-Coupled Receptor-2-Interacting Protein-1 Controls Stalk Cell Fate by Inhibiting Delta-like 4-Notch1 Signaling." Cell reports. 2016 Dec 6; 17(10):2532-2541.

5/2016
Hedberg-Buenz A, Christopher MA, Lewis CJ, Fernandes KA, Dutca LM, Wang K, Scheetz TE, Abramoff MD, Libby RT, Garvin MK, Anderson MG. "Quantitative measurement of retinal ganglion cell populations via histology-based random forest classification." Experimental eye research.. 2016 May 0; 146:370-85. Epub 2015 Oct 22.

3/2016
Fernandes KA, Bloomsburg SJ, Miller CJ, Billingslea SA, Merrill MM, Burgess RW, Libby RT, Fuerst PG. "Novel axon projection after stress and degeneration in the Dscam mutant retina." Molecular and cellular neurosciences.. 2016 Mar 0; 71:1-12. Epub 2015 Dec 10.

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