This is a very hot and extensively researched topic. Here is one approach to look at

Article: Exploiting mTOR Signaling: A Novel Translatable Treatment Strategy for Traumatic Optic Neuropathy?

Peter J Morgan-Warren, Martin Berry, Zubair Ahmed, Robert A H Scott, Ann Logan

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ABSTRACT: Retinal ganglion cell (RGC) death and a failure of axon regeneration contribute to the profound visual loss experienced by patients after traumatic optic neuropathy (TON), for which there are no effective treatments. Experimental manipulations of cellular signaling pathways in animal models have demonstrated that neuronal survival and axon regeneration in the mature central nervous system (CNS) are possible, and increased understanding of the molecular basis of prosurvival and regenerative signals has led to the identification of candidate targets for novel therapeutic strategies. The axogenic pathway is activated sequentially, after growth factor/receptor binding, through phosphoinositide-3-kinase (PI3K) and the downstream serine/threonine kinase Akt. Akt is a nodal point for the regulation of growth cone dynamics by glycogen synthase kinase (GSK3β) and axon protein synthesis/RGC survival by the mammalian target of rapamycin (mTOR). The mTOR signaling pathway has a pivotal role in numerous cellular processes. It is active during development, but downregulated in the mature CNS and further suppressed by axonal injury, and experimental upregulation of mTOR signaling promotes RGC survival and axon regeneration after optic nerve crush injury. However, several translational challenges remain, including understanding the regulatory mechanisms of axotomy-induced mTOR and GSK3β signaling, and the disparity between the RGC survival and axon regenerative effects. In this review, we explore the molecular basis of RGC regenerative failure and assess the potential for manipulations of mTOR signaling as a novel translatable treatment for TON.

Investigative ophthalmology & visual science 01/2013; 54(10):6903-16. ·

Dear Marianne, we have been studying retinal diseases for a few decades and in the last decade, have developed the use of save, non-invasive therapies with no side effects reported. These are dietary saffron and near-infrared light therapy. See my publications for example. I'm under Prof Jonathan Stone's group at Sydney Uni and he is the brains behind these studies using saffron and infrared light therapy for AMD, retinitis pigmentosa, Parkinson's disease and Alzheimer's disease. These therapies are said to be protective by reducing oxidative damage and switching on mitochondrial protective pathways.

Neuroprotection for the retinal ganglion cells will ultimately require both the prevention of RGC apoptosis after injury as well as the induction of a higher growth /proliferative state to repair damage to the axon. There are many promising approaches out there. One clinical trial in progress for ischemic optic neuropathy is designed to determine the efficacy of an siRNA that inhibits caspase 2 (which is an early activator of the apoptotic pathway).

Dear Dr. Prem Subramanian,

Good luck to you.