Diabetic retinopathy (DR) is the eye complication of diabetes. It affects up to 80% of patients who have suffered diabetes for more than 20 years. DR is caused by abnormalities in retinal blood vessels. The retinal vessel changes are initially non-proliferative in nature (non-proliferative DR, NPDR). With NPDR, the leakages of micro-vessels form macular edema. The micro-vessels could also close off, causing macular ischemia. Both forms of lesions could lead to the partial loss of vision or blurry. NPDR could gradually progress to more severe proliferative DR (PDR) as new blood vessels form in retina, which is called neovascularization. The newly formed vessels are usually fragile and often bleed into the vitroes. The bleeding could partially or completely block vision. Repeated disruption of retinal structure will lead to the scar formation and retinal detachment.
Most induced animal models of DR imitate only some features of DR, whereas spontaneous DR in NHPs recapitulates all the characteristics of human DR.
· Spontaneous DR has been identified in the diabetic monkeys at KBI. Both macular edema and ischemia were detected using fundus photograph (FP), fluorescein angiography (FA) and optical coherence tomography (OCT).
· Macular edema and ischemia can be also induced by laser at KBI and characterized using FP, FA and OCT.
Age-related macular degeneration (AMD) is a common eye disease that leads to the central vision loss among people age over 50. There are two types of AMD: dry (atrophic) and wet (neovascular or exudative). Most AMD starts as the dry type. Ten to 20% of AMD patients will progress to wet AMD.
AMD models at KBI are:
· Spontaneous in aged monkeys
· Blue light-induced (dry AMD)
· Argon laser-induced CNV (wet AMD)
The blood vessel leakage and retinal neovascularization are confirmed using fluorescein angiography (FA) and optical coherence tomography (OCT). Retinal lesions of CNV are determined and characterized using imaging analysis of FA.
Glaucoma, a leading cause of blindness, is a group of diseases that result in optical nerve damage. There are two forms of glaucoma: open-angle and closed-angle glaucoma. The open-angle form is usually caused by the slow drainage of aqueous humor from trabecular meshwork; the high intraocular pressure (IOP) caused by the accumulation of fluid in the front chamber of the eye results in the damage of optical nerve. The closed-angle form, a less common disease, is usually caused by the block of trabecular meshwork by iris. Although high IOP (>21 mmHg) is the most common risk factor for optical nerve damage, a good portion of people with high IOP never develop glaucoma; conversely, more than 50% of glaucoma patients (depending on their ethnic background) never develop high IOP.
NHP Glaucoma models available at KBI:
• Spontaneous glaucoma screened by IOP
Glaucoma 1.jpgGlaucoma 2.jpg
• Laser-induced open angle glaucoma
• Laser-induced normal tensive glaucoma
IOP is measured using TonoVet eye tonometer; Retinal Nerve Fiber Layer thickness (RNFLt) is analyzed using Optical Coherence Tomography (OCT); Retinal Ganglion Cell (RGC) function is assessed using Electroretinalgram (ERG).
Induced-eye disease models:
• Choroidal neovascularization (CNV, Wet AMD)
• Geographic atrophy (Dry AMD)
• OHT glaucoma
• Normal IOP glaucomatous neurodegeneration
• Retinal detachment
• Optic neuropathy Optic Neuritis
• Macular edema
• Low vision
Spontaneous eye disease models
• Drusen (Dry AMD)
• Dry eye