PRIYA CHAUDHARY, PH.D.
Dr. Chaudhary has worked on multiple neuroscience projects at Devers Eye, OR, New York Medical College, NY and Oregon Health & Science University (OHSU), OR. At Devers she is a co-investigator on two NIH grants to understand the remodeling at the optic nerve head (ONH). At OHSU she collaborated with various laboratories and clinicians as well as performed multidisciplinary research using in vivo and in vitro models.
For the past decade, she has investigated underlying molecular and cellular processes in multiple sclerosis (MS) with the goal of developing new treatment options. As a co-investigator on a VA Merit Review grant she investigated the effects of lipoic acid in murine experimental autoimmune encephalomyelitis (EAE), a model of MS. She has also worked on novel thyromimetic drugs that promote remyelination in MS and was extensively involved in an NIH grant that identified cyclophilin D, (CyPD), a mitochondrial permeability transition pore regulator, as a molecular target for neuroprotection in EAE.
Dr. Chaudhary’s long term goal is to investigate immunomodulatory and phagocytic mechanisms in neurodegenerative diseases. Currently, she is leading work on understanding how the ONH astrocyte cell biology and ONH connective tissue lead to biomechanic dysfunction in glaucoma.
Optic Nerve Head Myelin-Related Protein, GFAP, and Iba1 Alterations in Non-Human Primates With Early to Moderate Experimental Glaucoma.
A microwave method for plastic embedding of nervous tissue for light and electron microscopy.
Myelin repair stimulated by CNS-selective thyroid hormone action.
Effects of lipoic acid on primary murine microglial cells.
Glaucoma causes progressive loss of vision by damaging the optic nerve head tissues in the back of the eye. Advanced age is an important risk factor for developing glaucoma regardless of the level of intraocular (eye) pressure at which it occurs. Our research group and others have shown that experimental glaucoma causes alterations to the optic nerve head connective tissues and blood vessels which contribute to how the ganglion cell axons of the retina are damaged in this disease. But no one knows how this happens and so, to date, there are no medicines that directly prevent or treat this damage.
Our overarching hypothesis is that the optic nerve tissues are a demanding environment for the axons and that these tissues become more vulnerable in the aged eye. We plan to identify molecular and cellular components of optic nerve head (ONH) connective tissue and retrolaminar myelin remodeling in monkey early experimental glaucoma (EG). We will employ state of the art quantitative immunohistochemistry, electron microscopy, and precise anatomic colocalization of all microscopic findings to in vivo optical coherence tomography (OCT). We anticipate finding a robust glial cell immune modulation response in young eyes and decreased capacity for this response in aged eyes. We further anticipate that these experiments will confirm a role for ONH inflammation in glaucomatous vision loss. Once confirmed, these findings will lead to new vision preserving glaucoma therapies directed to the ONH tissues, complementing existing therapies that lower eye pressure.