About

Ala Moshiri, M.D., Ph.D., is a professor at UC Davis Health, specializing in ophthalmology with a focus on retina treatment and research. His clinical practice involves treating all forms of medical and surgical retinal diseases, including age-related macular degeneration, diabetic retinopathy, retinal vascular diseases, and inherited retinal conditions. He has expertise in eye injections and complex retinal surgeries such as retinal detachment, macular hole, and macular pucker. Dr. Moshiri dedicates a significant portion of his professional time to basic science research, where his team advances novel treatments like retinal cell replacement through photoreceptor transplantation and gene therapy for photoreceptor diseases. His research also explores retinal embryology and genetics to understand the molecular mechanisms underlying macular development, survival, and function. He holds degrees from UC Berkeley, the University of Washington, and completed his internship, residency, and fellowship at Johns Hopkins University. Dr. Moshiri emphasizes patient-centered care, respecting cultural sensitivities, and addressing healthcare disparities, especially for underserved and vulnerable populations.

Research topics

• Biology
• Surgery
• Medicine
• Genetics
• Ophthalmology
• Cell biology
• Neuroscience
• Computational biology
• Optometry
• Anatomy
• Evolutionary biology
• Internal medicine
• Endocrinology

Selected publications

• Rhesus macaques with an <i>OPA1</i> mutation demonstrate features of autosomal dominant optic atrophy

  Proceedings of the National Academy of Sciences · 2026-04-15

  articleOpen access

  Autosomal dominant optic atrophy (ADOA) is an inherited optic neuropathy primarily caused by mutations in OPA1 . We identified and defined a spontaneous nonhuman primate (NHP) model of ADOA using rhesus macaques heterozygous for a missense mutation ( OPA1 A8S). With ocular examinations, ophthalmic imaging, electroretinography, histopathology, immunohistochemistry, and transmission electron microscopy (TEM), we documented retinal nerve fiber layer (RNFL) thinning, retinal ganglion cell (RGC) loss and dysfunction, OPA1 mislocalization, and reduced axonal mitochondrial density in affected macaques. Our investigation revealed substantial phenotypic variability among affected macaques, shedding light on the pathogenesis of ADOA. The retinas were evaluated using techniques such as spectral-domain optical coherence tomography and fundus photography facilitating observation of structural changes in the retina and optic nerve. Thinning of the RNFL and optic nerve head degeneration, hallmark features of ADOA, were observed in affected macaques. Decreased RGC function in the OPA1 heterozygotes was demonstrated with pattern electroretinography. Histopathological analysis and immunohistochemical staining of postmortem retinal tissue suggested RGC loss in the papillomacular bundle, with reduced OPA1 and mitochondria in the RGC axons, indicating dysfunctional mitochondrial dynamics and reduced function consistent with ADOA. Ultrastructural changes were evident with TEM including dysmorphic mitochondria, axonal loss, myelin disruption, and hypertrophic astrocytic processes. The observed similar pattern of RGC loss and dysfunction coupled with phenotypic heterogeneity in our NHP model reflects the clinical variability observed in human ADOA patients indicating that therapeutic interventions in this foveate model will likely translate to the human condition.

  PublisherDOI

• Combined Mouse Retinal Optoretinography/Electroretinography System to Study Light-Evoked Responses in Animal Models of Retinal Degeneration

  Investigative Ophthalmology & Visual Science · 2026-01-20 · 1 citations

  articleOpen access

  Purpose: To study the correlation between optoretinogram (ORG) and the underlying phototransduction-initiated physiology, we irradiated mouse retinas with visible light centered at a 482-nm wavelength to induce bleach-initiated morphologic changes in the outer retinal layers, including photoreceptors and the retinal pigment epithelium (RPE). Methods: A 482-nm light-emitting diode was used for short-pulse irradiation of the retina over a large field of view in the three groups of mice, including disease models, while acquiring optical coherence tomography (OCT) image sequences using a custom-built OCT system combined with a commercial electroretinogram (ERG) system. The visible light exposure was adjusted to vary the total light energy (number of photons) delivered to the retina, enabling observation of the bleach-level dependence of the ORG and ERG signals. Results: Light-driven thickness increments in the outer retinal layers, including the photoreceptors and RPE, were observed in wild-type (WT) albino and pigmented mice. However, the energy of light stimuli did not produce a response in the retina of the rd10 mouse model. The lack of a full-field ERG response in the same animals also confirmed this observation. These suggested that phototransduction in the 3-month-old rd10 mice could not be initiated. Conclusions: The ORG and ERG measurements recorded under various light stimuli reveal the retina's neural function. The ORG and ERG signals from the WT albino and pigmented mice exhibited thickness increments in the ORG and an increase in amplitude of a-waves and b-waves in the ERG, which were linked to phototransduction; however, these signal trends were not observed in the rd10 mice. Therefore, the ORG/ERG system could be an attractive instrument that provides both localized structural and global functional information about the investigated retina, allowing for detailed studies of neural function suppression in animal models of retinal degeneration.

  PublisherDOI

• Illuminating retinoid flux in the neurosensory retina

  Journal of Clinical Investigation · 2026-02-01

  articleOpen access1st authorCorresponding

  The retinoid chromophore 11-cis-retinal triggers an intracellular cascade known as phototransduction that converts light into electrochemical signals. Enzymatic regeneration of 11-cis-retinal sustains vision, prevents the buildup of toxic byproducts, and is supported largely by the retinal pigmented epithelium. Directly visualizing rapidly changing retinoid intermediates in patients with inherited retinal diseases (IRDs) could provide essential therapeutic insights. In this issue, Engfer et al. introduced a groundbreaking strategy using the mouse retina as a genetically malleable model for the mammalian eye. Using cell-specific expression of lecithin:retinol acyltransferase to trap mobile retinols, they mapped the availability of 11-cis- and all-trans-retinoids within different retinal compartments under normal and diseased conditions. Their findings elucidate retinoid distribution in the retina and highlight important differences between mouse and human Müller glia. Here, we contextualize these advances within decades of research defining the visual cycle and retinoid biology, outlining the profound implications for therapeutic development for IRDs.

  PublisherDOI

• Retinal Detachment in Incarcerated Patients

  Journal of VitreoRetinal Diseases · 2025-09-10 · 1 citations

  articleOpen access

  Purpose: To describe the clinical characteristics and outcomes of incarcerated patients with rhegmatogenous retinal detachment (RRD). Methods: This is a retrospective case series of incarcerated patients evaluated at the University of California, Davis Medical Center. Results: Twenty-five patients (25 eyes) were included in the study. The mean (±SD) duration of symptoms prior to presentation was 41 ± 105.3 days, and a history of trauma was reported in 12 (48%) patients. Mean preoperative logMAR visual acuity was 1.9 ± 0.2, and this improved to 1.3 ± 0.2 ( P = .034) at last follow-up (mean follow-up, 9.4 ± 4.5 months). Single-surgery success was achieved in 9 patients (56.3%) with 3 months or more of follow-up. Conclusions: A significant proportion of incarcerated patients with RRD report a history of trauma and present for care after significant delay. Prompt access to care may improve outcomes.

  PublisherOA PDFDOI

• Genome-Wide Insights Into the Genes and Pathways Shaping Human Foveal Development: Redefining the Genetic Landscape of Foveal Hypoplasia

  Investigative Ophthalmology & Visual Science · 2025-09-09 · 3 citations

  articleOpen access

  Purpose: To define the genetic architecture of foveal morphology and explore its relevance to foveal hypoplasia (FH), a hallmark of developmental macular disorders. Methods: We applied deep-learning algorithms to quantify foveal pit depth from central optical coherence tomography (OCT) B-scans in 61,269 UK Biobank participants. A genome-wide association study (GWAS) was conducted using REGENIE, adjusting for age, sex, height, and ancestry. Rare coding variants (frequency <1%) were analyzed in an exome-wide rare-variant association study (RVAS). Candidate genes were prioritized using integrative mapping; pathway, cross-ancestry, and genetic-correlation analyses were exploratory. Results: GWAS identified 126 sentinel variants, including 47 novel associations. Integrative mapping prioritized 129 putative causal genes, with 64 not previously implicated in foveal biology. Enriched pathways included retinoic acid metabolism (e.g., CYP26A1), photoreceptor differentiation (e.g., VSX2), extracellular matrix organization, and pigmentation. RVAS identified missense variants in ACTN3 and ESYT3 (P < 5 × 10-⁹) associated with FH features. Polygenic scores were predictive across African and South Asian ancestries. Overlap was observed with monogenic FH genes (TYR, OCA2, PAX6, AHR) and with genes underlying systemic diseases (COL11A1, KIF11, TUBB4B, PHYH). Re-examination of OCTs in affected individuals confirmed FH in select cases, including those with recurrent TUBB4B p.(Arg390Trp) variants. Conclusions: This is the first GWAS of human foveal morphology. Our findings redefine the genetic and biological framework underlying normal foveal development and foveal hypoplasia (FH). By linking common variation to rare monogenic disease, we establish a continuum model of FH with implications for future mechanistic and clinical investigation.

  PublisherOA PDFDOI

• Randomized Study of Intravitreal Autologous CD34+ Stem Cells in Central Retinal Vein Occlusion (Treatment of Retinal vein occlusion Using STem cells [TRUST] Report 1): Safety and Feasibility

  Ophthalmology Science · 2025-08-05

  articleOpen access

  Purpose: To assess the safety and feasibility of intravitreal injection of autologous CD34+ bone marrow stem cells (BMSCs) in eyes with vision loss from central retinal vein occlusion (CRVO). Design: Phase I/II single-center, prospective, randomized, sham-controlled, double-masked study. Participants: Participants with CRVO of 6 to 42 months duration, best-corrected visual acuity (VA) of 20/40 to 20/400, and no concurrent retinopathy or optic neuropathy contributing to vision loss in the study eye. The exclusion criteria include any concurrent systemic condition that would alter bone marrow components. Methods: Participants were randomized to immediate cell injection followed by sham injection at month 6 or immediate sham injection followed by cell injection at month 6. Cell injection consisted of a bone marrow aspiration and intravitreal injection of autologous CD34+ BMSCs. CD34+ BMSCs were isolated from the mononuclear cell fraction of bone marrow using Miltenyi CliniMACS system under current good manufacturing practices. Isolated cells were released for intravitreal injection if they passed the release criteria for quantity, sterility, and viability accepted by the US Food and Drug Administration. Sham injection consisted of a sham bone marrow aspiration and intravitreal injection without entering bone or eye. Eye examination, microperimetry, fundus photography, fluorescein angiography, electroretinography, OCT, and OCT angiography were performed at baseline and during study follow-up of 12 months. Main Outcome Measures: Adverse events (AEs) associated with study treatment, number of CD34+ BMSCs injected intravitreally. Results: Sixteen participants (16 eyes) were randomized to 1 of 2 study groups. All received intravitreal injection of autologous CD34+ BMSCs (mean 4.3 million cells) and completed the study follow-up. Rubeosis with vitreous hemorrhage occurred in 1 study eye, <1 month after sham injection and 7 months after cell injection, attributed to normal progression of CRVO. There were no other serious ocular AEs. The most common AE related to the study cell injection was new floaters (15/16, 93%). Other ocular AEs were similarly noted after sham injection. No eye had persistent VA loss of ≥15 letters after cell injection. Conclusions: Intravitreal injection of autologous CD34+ BMSCs appears well-tolerated and feasible in eyes with vision loss from CRVO. Financial Disclosures: Proprietary or commercial disclosure may be found in the Footnotes and Disclosures at the end of this article.

  PublisherDOI

• Ocular Phenotyping of Knockout Mice Identifies Genes Associated With Late Adult Retinal Phenotypes

  Investigative Ophthalmology & Visual Science · 2025-06-23 · 1 citations

  articleOpen accessSenior authorCorresponding

  Purpose: Analyze phenotypic data from knockout mice with late-adult retinal pathologic phenotypes to identify genes associated with development of adult-onset retinal diseases. Methods: The International Mouse Phenotyping Consortium (IMPC) database was queried for genes associated with abnormal retinal phenotypes in the late-adult knockout mouse pipeline (49-80 weeks postnatal age). We identified human orthologs and performed protein-protein analysis and biological pathways analysis with known inherited retinal disease (IRD) and age-related macular degeneration (AMD) genes using Search Tool for the Retrieval of Interacting Genes/Proteins (STRING), PLatform for Analysis of single cell Eye in a Disk (PLAE), Protein Analysis Through Evolutionary Relationships (PANTHER), and Kyoto Encyclopedia of Genes and Genomes (KEGG). Results: Screening of 587 late-adult mouse genes yielded 12 with abnormal retinal phenotypes, which corresponded to 20 human orthologs. Three of the 12 mouse genes and two of the 20 human orthologs were previously implicated in retinal pathology or physiology in a literature review. Although all of the genes demonstrated retinal pathology when deleted from the mouse genome, most do not have established roles in human retinal disease. Furthermore, human protein-protein analysis and biological pathway analysis yielded only a few relationships between the candidate gene list and that of known IRD and AMD genes, suggesting they may represent novel retinal functions. Conclusions: We identified 12 mouse genes with significant late-adult abnormal retinal pathology, eight of which have not been previously implicated in either mouse or human retinal physiology or pathology. These serve as novel retinal disease gene candidates for late-onset retinal disease.

  PublisherOA PDFDOI

• Systematic Ocular Phenotyping of Knockout Mouse Lines Identifies Genes Associated With Age-Related Corneal Dystrophies

  Investigative Ophthalmology & Visual Science · 2025-05-05 · 1 citations

  articleOpen accessSenior authorCorresponding

  Purpose: This study investigates genes contributing to late-adult corneal dystrophies (LACDs) in aged mice, with potential implications for late-onset corneal dystrophies (CDs) in humans. Methods: The International Mouse Phenotyping Consortium (IMPC) database, containing data from 8901 knockout mouse lines, was filtered to include late-adult mice (49+ weeks) with significant (P < 0.0001) CD phenotypes. Candidate genes were mapped to human orthologs using the Mouse Genome Informatics group, with expression analyzed via PLAE and a literature review for prior CD associations. Comparative analyses of LACD genes from IMPC and established human CD genes from IC3D included protein interactions (STRING), biological processes (PANTHER), and molecular pathways (KEGG). Results: Analysis identified 14 genes linked to late-adult abnormal corneal phenotypes. Of these, 2 genes were previously associated with CDs in humans, while 12 were novel. Seven of the 14 genes (50%) were expressed in the human cornea based on single-cell transcriptomics. Protein-protein interactions via STRING showed several significant interactions with known human CD genes. PANTHER analysis identified six biological processes shared with established human CD genes. Two genes (Rgs2 and Galnt9) were involved in pathways related to human corneal diseases, including cGMP-PKG signaling, mucin-type O-glycan biosynthesis, and oxytocin signaling. Other candidates were implicated in pathways such as pluripotency of stem cells, MAPK signaling, WNT signaling, actin cytoskeleton regulation, and cellular senescence. Conclusions: This study identified 14 genes linked to LACD in knockout mice, 12 of which are novel in corneal biology. These genes may serve as potential therapeutic targets for treating corneal diseases in aging human populations.

  PublisherOA PDFDOI

• #ECR-Paper-05 Genome-wide insights into the genes and pathways shaping human foveal development

  2025-10-01

  articleOpen access

  a key feature of conditions such as

  PublisherOA PDFDOI

• Genome-Wide Insights into the Genes and Pathways Shaping Human Foveal Development

  medRxiv · 2025-06-20

  preprintOpen access

  Abstract Here we report the first genome-wide association study of foveal pit depth. In a cohort of 61,269 individuals, we identified 123 genome-wide significant loci associated with pit depth, including 47 novel associations not previously linked to macular traits. Using 12 complementary variant-to-gene mapping strategies, we prioritised 128 putative causal genes, 64 of which have not previously been implicated in foveal development. Our findings reveal previously unrecognised biological influences on foveal morphogenesis, including retinoic acid metabolism (implicating CYP26A1 for the first time in human foveal development), extracellular matrix and cytoskeletal dynamics, and retinal cell fate determination. In addition, rare-variant analysis uncovered two further gene associations, including ESYT3 , a gene not previously linked to foveal structure. Together, these results provide new insights into the genetic architecture and molecular pathways underlying human foveal development, and offer a foundation for future functional studies aimed at characterising foveal development and disease.

  PublisherOA PDFDOI

Recent grants

• The Role of ARAP1 in Retinal Photoreceptor Homeostasis

  NIH · $1.0M · 2017–2022

Frequent coauthors

• Glenn Yiu

  University of California, Davis

  42 shared

• Sara M. Thomasy

  University of California, Davis

  37 shared

• Rui Chen

  Baylor College of Medicine

  32 shared

• Susanna S. Park

  University of California, Davis

  32 shared

• Jeffrey Rogers

  Baylor College of Medicine

  28 shared

• Lawrence S. Morse

  West Virginia University

  24 shared

• Yann Hérault

  Université de Strasbourg

  20 shared

• Christopher J. Murphy

  16 shared

Awards & honors

• The Arnall J. Patz Research Grant Award (2011)
• The Ray Sjaarda Research Grant Award (2009)
• The Susan Bressler Research Grant Award (2007)
• Achievement Rewards for College Scientists (ARCS) Foundation…