About

Ana Ross, Ph.D., is an Assistant Professor of Clinical Psychiatry at the Children's Hospital of Philadelphia. She is a psychologist in the Department of Child and Adolescent Psychiatry and Behavioral Sciences. Her educational background includes a BS in Psychology and Political Science from Pennsylvania State University, obtained in 2015, an MA in School Psychology from the University of Maryland in 2019, and a Ph.D. in School Psychology from the University of Maryland in 2021. Her research focuses on youth mental health, telehealth services, and medical procedures desensitization for individuals with Autism Spectrum Disorder. She has contributed to the field through various presentations and publications related to pediatric psychology, mental health promotion, and the impact of COVID-19 on mental health services.

Research topics

• Medicine
• Political Science
• Biology
• Environmental health
• Sociology
• Nursing
• Gerontology
• Family medicine
• Genetics
• Neuroscience
• Ophthalmology
• Surgery
• Business
• Medical education
• Economic growth
• Law
• Evolutionary biology
• Demography
• Optometry

Selected publications

• A Remarkable Tale: Increased Retinal Fluorescence Following Application of Permanent Marker Ink to Mouse Tails

  Investigative Ophthalmology & Visual Science · 2026-03-17

  articleOpen access

  Purpose: Unusually high retinal fluorescence was observed during in vivo imaging among a few mice in our colony. Their tails had been marked with red Sharpie ink, a common practice for identification. They were observed licking the ink off their tails, suggesting possible oral intake of a fluorescent ink component that might accumulate in the retina. One component of red marker ink is the fluorophore Rhodamine 6G (R6G), suggesting that it might be responsible. Methods: We tested this hypothesis by tail marking C57Bl/6J mice with one line or four lines of red ink. Retinal fluorescence was monitored in vivo with confocal scanning laser ophthalmoscope (cSLO) imaging at baseline and from 6 hours to 2 weeks after marking. Retinas and brains were sectioned for histology. A second cohort of mice received an oral gavage of R6G at the concentration estimated in red ink, and retinal histology was performed. Results: Tail marking with red ink led to a transient, dose-dependent increase in retinal fluorescence in cSLO images, peaking at 6 hours. Histology revealed that this fluorescence was predominantly in the photoreceptor outer segments. This fluorescence localization was reproduced with oral R6G alone. Fluorescence in the brain was concentrated in the choroid plexus and ventricles. Conclusions: These results suggest that R6G can cross the gut-blood, blood-retina, and blood-cerebrospinal fluid barriers. This raises important technical considerations for experimental mouse identification and has potential applications for fluorescence imaging and central nervous system drug targeting.

  PublisherDOI

• Variant-to-gene mapping identifies <i>ARHGEF12</i> as a primary open-angle glaucoma effector gene operating within retinal ganglion cells

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-02-23 · 1 citations

  articleOpen access

  Abstract Primary open-angle glaucoma (POAG), a leading cause of irreversible blindness, has a strong genetic basis. The Primary Open-Angle African Ancestry Glaucoma Genetics study previously identified 46 risk loci. To pinpoint causal variants and their corresponding effector genes, we analyzed gene expression, chromatin accessibility, and conformation in two ocular cell-types: trabecular meshwork cells (hTMCs) and retinal ganglion cells derived from induced pluripotent stem cells (hiPSC-RGCs). We identified 24 candidate genes in hTMCs and 56 in hiPSC-RGCs. The ARHGEF12 gene was selected for further validation because it was nominated by local and distal promoter interactions in both cell-types and has reproducible prior evidence of its association with POAG. While its role in hTMCs is established, its function in RGCs is unclear. hiPSC-RGCs generated from a POAG donor homozygous for the risk allele showed reduced ARHGEF12 expression, altered morphology, and disrupted neuronal activity. This framework enables functional evaluation of additional POAG risk variants.

  PublisherDOI

• Neuroprotective effects of SIRT1 in human RGCs derived from iPSCs following oxidative stress induction at early and late stages of differentiation

  Experimental Eye Research · 2025-07-17 · 1 citations

  articleOpen accessSenior authorCorresponding

  BACKGROUND: Neurodegeneration of retinal ganglion cells (RGCs) is the primary cause of irreversible vision loss in optic neuropathies. Preclinical in vivo studies have shown the neuroprotective potential of SIRT1 gene therapy in various optic neuropathy mouse models. This study seeks to build on these findings by utilizing a human cell culture model of induced pluripotent stem cell (iPSC)-derived RGCs to assess the neuroprotective effects of SIRT1 expression. METHODS: RGCs were differentiated from control human iPSCs using a previously defined in vitro methodology with small molecules and peptide modulators. Cell morphology and identity was confirmed by Brn3a and RBPMS immunostaining as well as qPCR analysis of RGC-specific markers. SIRT1 and GFP (control) were expressed using AAV vectors driven by the RGC-selective SNCG promoter. Oxidative stress was induced using tert-butyl hydroperoxide solution (TBHP) or growth factor withdrawal, and neuroprotection was assessed via MTT assay. RESULTS: By day 42 of differentiation, cultures were enriched with Brn3a + cells (>80 %) that demonstrated morphologic features of mature RGCs, and these RGC properties were maintained up to day 90. SIRT1 expression induced significant neuroprotection to human iPSC-derived RGCs following TBHP-induced oxidative stress and with depletion of growth factors. Rescue effects were observed within three weeks of SIRT1 expression, with improved RGC survival compared to controls (∼20 %), at two timepoints: Days 42 and 90. CONCLUSIONS: These findings support the therapeutic success of SIRT1-based gene therapy in an in vitro culture model of human RGCs and confirm those obtained in mouse models of optic neuropathies.

  PublisherDOI

• A multi-cohort genome-wide association study in African ancestry individuals reveals risk loci for primary open-angle glaucoma

  UNC Libraries · 2025-02-01

  articleOpen access
  PublisherDOI

• Mitochondrial Uncoupler, 2,4-Dinitrophenol, Reduces Spinal Cord Paralysis and Retinal Ganglion Cell Loss in the Experimental Autoimmune Encephalomyelitis Model of Multiple Sclerosis

  Biomolecules · 2025-01-28 · 1 citations

  articleOpen access

  Optic neuritis is an inflammatory demyelinating disease of the optic nerve that often occurs in multiple sclerosis (MS) patients. Sixty percent of patients develop some level of permanent visual loss due to retinal ganglion cell (RGC) damage following optic neuritis, with no known treatment to prevent this loss. Prior studies showed that MP201, a prodrug of 2,4-dinitrophenol (DNP) administered in the experimental autoimmune encephalitis (EAE) mouse model of MS attenuated optic neuritis with preserved vision, increased retinal ganglion cell (RGC) survival, decreased axon loss, and reduced demyelination. Oral administration of MP201, which converts to active form DNP after entry in the portal vein, decreases mitochondrial-derived reactive oxygen species (ROS) and restores calcium homeostasis, which are both implicated in many neurodegenerative diseases. Due to the established therapeutic benefits of prodrug MP201 in EAE mice, we hypothesized that administration of DNP itself may also have significant potential for therapeutic effects. Here, effects of varying doses of DNP treatment in EAE mice were assessed by the extent of spinal cord paralysis, optokinetic response (OKR), RGC survival, and optic nerve demyelination and inflammation. Results show that daily oral doses of 5-10 mg/kg DNP initiated after onset of EAE can significantly reduce spinal cord paralysis, a marker of the EAE MS-like disease, by day 42 after disease induction. DNP treatment significantly reduces RGC loss induced by optic neuritis in EAE mice; however, effects of DNP do not significantly improve visual function, or optic nerve demyelination and inflammation. Current studies show DNP treatment promotes increased RGC survival, but continued inflammation and demyelination likely reduce visual function, suggesting future studies examining combination therapy of DNP with anti-inflammatory agents may be warranted.

  PublisherOA PDFDOI

• Response to comment on “Neuroprotective effects of SIRT1 in human RGCs derived from iPSCs following oxidative stress induction at early and late stages of differentiation”

  Experimental Eye Research · 2025-08-21

  letterSenior authorCorresponding
  PublisherDOI

• SIRT1-based therapy targets a gene program involved in mitochondrial turnover in a model of retinal neurodegeneration

  Scientific Reports · 2025-04-19 · 6 citations

  articleOpen access

  Neurodegenerative diseases of the eye such as optic neuritis (ON) are hallmarked by retinal ganglion cell (RGC) loss and optic nerve degeneration leading to irreversible blindness. Therapeutic interventions enhancing expression or activity of SIRT1, an NAD+-dependent deacetylase, support, at least in part, survival of RGCs in the face of injury. Herein, we used mice with experimental autoimmune encephalomyelitis (EAE) which recapitulates axonal and neuronal damages characteristic of ON to identify gene regulatory networks affected by constitutive ubiquitous Sirt1 expression in SIRT1 knock-in mice and wild-type mice upon targeted adeno-associated virus (AAV)-mediated SIRT1 expression in RGCs. RNA seq data analysis showed that the most upregulated genes in EAE mouse retinas include those involved in inflammation, immune response, apoptosis, and mitochondrial turnover. The latter includes genes regulating mitophagy (e.g., Atg4), mitochondrial transport (e.g., Ipo- 6, Xpo- 6), and mitochondrial localization (e.g., Chrna4, Scn9a). The constitutive or RGC-targeted SIRT1 overexpression in EAE mice upregulated the expression of non-mitochondrial genes such as Ecel1 and downregulated the expression of mitophagy genes (e.g., Atg2b, Arifip1) which were upregulated by EAE alone. Thus, SIRT1 induces neuroprotection by, at least in part, balancing mitochondrial biogenesis and mitophagy and/or enhancing mitochondrial self-repair to preserve the bioenergetic capacity of RGCs.

  PublisherOA PDFDOI

• Neuroprotective Effects of Sirt1 in Human Rgcs Derived from Ipscs Following Oxidative Stress Induction at Early and Late Stages of Differentiation

  SSRN Electronic Journal · 2025-01-01

  preprintOpen accessSenior author
  PublisherDOI

• Gender Differences in Patient-Physician Communication in Ophthalmic Practice, Pre- and Post-COVID-19 Period

  American Journal of Ophthalmology · 2025-03-15

  articleOpen access

  PURPOSE: Physician communication patterns can increase patient satisfaction and adherence to therapy in the primary care setting. This study investigated gender differences in ophthalmologist communication patterns before and after the COVID-19 pandemic. DESIGN: Retrospective cohort study. METHODS: Messages sent by ophthalmic patients at Penn Medicine from 2017 to 2022 were collected. Differences in the number of physician messages sent for a given patient, median response length, and response time to patient inquiries and messages were examined based on year and physician gender. RESULTS: Female ophthalmologists sent longer response messages to their patients (median [25th, 75th percentiles] response length for women vs men: 672 [492-965] characters vs 637 [460, 918] characters; P < .0001) and a higher number of response messages per patient than their male counterparts (mean [SD] for women vs men: 5.5 [2.9] vs 3.0 [1.5]; P = .04). There was an increase in this gender difference in the peri- and post-COVID-19 period (ie, 2020-2022) (P = .007). Male ophthalmologists sent a higher percentage of same-day responses from 2017 to 2020 (P < .0001), whereas female ophthalmologists sent a higher percentage of same-day responses from 2021 to 2022 (P < .0001). The largest gender difference in same-day responses occurred in 2020 (34% for men vs 30% for women; P < .0001). CONCLUSIONS: Gender differences exist in ophthalmologist communication patterns, and the COVID-19 pandemic impacted these differences. Future studies will be helpful in determining the potential association of these specific communication patterns with patient satisfaction assessments, eye health outcomes, and physician burnout.

  PublisherDOI

• AAV2 vector optimization for retinal ganglion cell-targeted delivery of therapeutic genes

  Gene Therapy · 2024-01-10 · 9 citations

  articleSenior author
  PublisherDOI

Recent grants

• The Development of Gene Therapy Using SIRT1 Signaling to Treat Chronic Glaucoma

  NIH · $958k · 2019–2023

Frequent coauthors

• Kenneth S. Shindler

  Penn Presbyterian Medical Center

  97 shared

• Maxwell Pistilli

  University of Pennsylvania

  64 shared

• Madhura A. Tamhankar

  California University of Pennsylvania

  60 shared

• Grant T. Liu

  University of Pennsylvania

  59 shared

• Imran Jivraj

  University of Alberta

  52 shared

• Zoë R. Williams

  University of Rochester Medical Center

  49 shared

• Gregory P. Van Stavern

  49 shared

• John J. Chen

  Mayo Clinic

  49 shared

Labs

• Ana Ross LabPI

Education

• Assistant Professor, Ophthalmology and Neurology

  University of Pennsylvania

• MD PhD, Medical School

  Thomas Jefferson University

  2011

• BA, Chemisrty

  Bryn Mawr College

  2003