Disease Models

Retinitis Pigmentosa

Progressive thinning of the outer nuclear layer (ONL), loss of definition in the external limiting membrane (ELM), and disapearance of the photoreceptor inner and outer segment (IS/OS) junction.

Diabetic Retinopathy

Early neurodegenerative thinning of the ganglion cell complex (GCC) and inner plexiform layers (IPL) due to chronic high blood sugar levels. Later diffuse edema and advanced inflammation disrupts the sharp clear boundaries of the retina.

Wet Age Related Macular Degeneration

Laser burns rupture Bruch's membrane (BM) triggering rapid and abnormal blood vessel growth into the subretinal space. This laser-induced choroidal neovascularization results in choroidal sprouting of leaky vessels that lift the retina from the RPE.

Glaucoma

Retinal nerve fiber layer (RNFL) thinning shows early loss of cell axons, while optic nerve head (ONH) cupping creates visible depression as tissue dies. The ganglion cell complex (GCC) thins with the death of inner retinal neurons.

Dry Age Related Macular Degeneration

The retinal pigment epithelium (RPE) and Bruch's membrane (BM) become uneven, thinned, or fragmented causing the outer nuclear layer (ONL) to shrink as photoreceptor cells die. Small drusen-like elevations form below the RPE.

Corneal Wound Healing

Epithelial gaps and stromal swelling caused by chemically or physically induced wounds can be measured and tracked with both OCT and OCTA to capture scarring, opacities, and corneal neovascularization as distress signals prompt new vessels and myofibropblasts to rush in.