Photoreceptor transplantation as a treatment for retinal disease

Introduction

The retina, as part of the central nervous system (CNS), is made up of neurons which degenerate progressively throughout life.

Like elsewhere in the CNS, retinal neurons in the mammalian class of vertebrates have little ability to regenerate or repair after injury – a problem that has perplexed experimental neurologists for well over a century [1].

In recent decades, however, it has become apparent that the mammalian visual pathway still exhibits considerable plasticity. In rodents, adult retinal ganglion cells can regenerate along a peripheral nerve graft to form functional synapses in the tectum [2-4] and during late development, ganglion cells can regenerate and navigate through the optic chiasm in a marsupial mammal [5].

These observations and others confirm that the adult visual pathway is capable of reforming new synapses and may have a capacity to guide navigation of regenerating axons in certain circumstances. In other words, if regenerating neurons are presented to the adult diseased CNS and the correct conditions are met, there is no scientific reason to presume that the host CNS will not accept new synapses with the capability to restore function.

Hence the onus for CNS repair shifts to the donor cell and the problem becomes one of obtaining large enough numbers of these cells at the correct developmental stage to optimise any functional benefit following transplantation into the diseased CNS. Until recently this was the limiting step for any clinical applications since embryonic stem cells have ethical restrictions and would in any case most likely be rejected after neuronal differentiation without immune suppression.

The generation and subsequent neuronal differentiation of induced pluripotent stem (iPS) cells, however, has removed many of these limitations and it is appropriate now for clinicians to begin considering which diseases might be applicable for early clinical trials.

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Source: Robert E. MacLaren

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