Boosting Mitochondria- A New Approach For Protecting The Aging Optic Nerve In Glaucoma
Funder
National Health and Medical Research Council
Funding Amount
$391,784.00
Summary
Increasing age is a major risk factor for neurodegeneration. We have recently shown that subjecting mice to intermittent periods of fasting improves mitochondrial function in the retina and reverses age-related decline in optic nerve vulnerability to injury. This project now aims to investigate key molecular pathway for restoring mitochondria and from this attempts to find more palatable therapeutic strategies for protecting the optic nerve from injury.
Do Activated Retinal Microglia Mediate Neurotoxicity In Background Diabetic Retinopathy?
Funder
National Health and Medical Research Council
Funding Amount
$435,589.00
Summary
Diabetic retinopathy, a frequent complication of Type 1 and Type 2 diabetes, is the commonest cause of blindness in working age individuals. Prior to the growth of blindness-causing new vessels in the eye we now know that there is a gradual loss of neurons in the retina. This project will investigate whether the resident immune cells in the retina, which are normally neuroprotective, become neurotoxic during episodes of systemic inflammation (e.g. bacterial or viral infections).
Investigating Trans-synaptic Degeneration In The Human Visual Pathway
Funder
National Health and Medical Research Council
Funding Amount
$79,514.00
Summary
This research project investigates the spread of neuronal damage along the visual pathway from the retina to higher order areas including the visual cortex and inter-hemispheric tracts. This trans-synaptic degeneration will be examined in Leber's optic atrophy, optic neuritis and glaucoma.
Investigating The Mechanisms Underpinning The Dynamic Vessel Response In People With Diabetic Retinopathy
Funder
National Health and Medical Research Council
Funding Amount
$18,808.00
Summary
Endothelial dysfunction has been well-hypothesised as one of the key players in the pathogenesis of DR. However, there is strong evidence suggesting a neurovascular coupling mechanism in the retinal circulation during flicker. It is therefore unclear whether reduced flicker light induced vasodilation observed in diabetes and DR is associated with endothelial dysfunction, an impairment of neurovascular coupling or both. This project aims to address this important knowledge gap.
Oxidative Phosphorylation Regulation And Neuroprotection In Optic Neuropathies
Funder
National Health and Medical Research Council
Funding Amount
$430,231.00
Summary
We have shown clear differences in the mitochodria, cellular organelles that generate energy, between optic atrophy patients who have good vision and those of patients who have poor vision. We believe that these changes represent a compensation mechanisms that preserves mitochondrial energy production and protects optic nerve cells. This study will characterize these differences further with the aim of identfying new treatments for preventing nerve loss and preserving vision.