[2] He is known for his research on the mechanisms of uveitis,[3][4] non-visual photoreception in the eye,[5] and vision-restoration methods for retinal degenerative disease,[6][7] as well as his leadership and advisory positions in various American ophthalmological and medical societies.
[11] He then completed an internal medicine internship at Stanford before moving to Washington University in St. Louis/Barnes-Jewish Hospital in 1995, where he was a resident in the Department of Ophthalmology and Visual Sciences.
[15] The Van Gelder lab is investigating synthetic small molecule switches as a therapeutic for degenerative blinding diseases (such as age-related macular degeneration, which is caused by death of rods and cones).
Dr. Van Gelder's 1990 PNAS paper is one of his most influential and highly cited contribution to the fields of neuroscience and recombinant DNA technology.
Mark von Zastrow and James Eberwine, Van Gelder developed a technique called antisense RNA amplification that was able to generate amplified RNA populations from limited amounts of cDNA in order to obtain ample amounts of nucleic acid needed for standard cloning techniques.
Using a micro-electrode array in the ipRGCs of murine mice, Dr. Van Gelder found that there are three distinct cell populations in the postnatal day 8 (P8) retina, varying in their speed of onset, offset, and sensitivity.
[19] In a 2015 PNAS paper, Dr. Van Gelder and colleagues (with first author former postdoctoral fellow Ethan Buhr) found that Opsin-5 is sufficient for the entrainment of the molecular circadian clock in the mammalian retina.
Additionally, Dr. Van Gelder's lab found that OPN5 was sufficient in entraining the circadian rhythms of mice cornea ex-vivo, ascertaining the function of OPN5, which until then was classified as an orphan opsin.
Dr. Van Gelder's work in this field has included the use of spectral-domain optical coherence tomography (SD-OCT), which involves the use of a line-scan camera, instead of a spectrometer as is conventionally used in OCT.