Blind World


Retinitis Pigmentosa.
Spinach pigments proposed as blindness cure.





May 4, 2004.

By Duncan Graham-Rowe,
New Scientist.




A truly extraordinary cure for some forms of blindness is being proposed. The idea is to add light-absorbing pigments from spinach to nerve cells in the retina, to make the nerve cells fire when struck by light.


Eli Greenbaum's team at the Oak Ridge National Laboratories in Tennessee has been exploring this possibility for several years. In their latest experiments, the researchers have shown that adding plant pigments to human cells makes the cells respond to light.


The technique would restore only limited vision at best - people would be colour-blind, for instance - but Greenbaum thinks it could provide far better resolution than the electronic retinal implants being developed.


Restoring vision.


Degenerative diseases of the retina such as retinitis pigmentosa and macular degeneration are among the most common forms of blindness in developed countries. These diseases affect rods and cones, the photoreceptor cells at the back of the retina, but the nerve cells in front of them usually remain intact.


Experiments with implants that consist of an array of electrodes have shown it is possible to restore at least rudimentary vision by stimulating these nerve cells directly (New Scientist print edition, 23 November 2002).


Electric potential.


"Taking our cue from these clinical results, we aim to replace voltage stimulation by electrodes with voltage stimulation by the photosystem I reaction centres," says Greenbaum. Each PSI reaction centre is a cluster of proteins that straddles the chloroplast membrane in plant cells. The centres play a key role in photosynthesis, generating an electric potential when struck by light.


In 2001 Greenbaum's team inserted PSI centres, isolated from spinach, into the membranes of fatty spheres called liposomes, which are used to deliver drugs or genes to cells. The researchers found that the voltage generated across the liposome membrane when the complexes absorb light exceeds the threshold needed to make a nerve cell fire.


Now the team has carried out the next step, using the liposomes to add the PSI complexes to membranes of eye cancer cells called retinoblastomas. When the cells were exposed to light, calcium ion channels opened up in the membrane.


The results, which will be presented at the Biosensors 2004 conference in Spain in April, show that adding PSI centres does at least make cells respond to light.


Series of reactions.


But this does not prove that adding PSI centres to the bipolar and ganglia cells in the retina would make them fire when hit by light, other experts point out. "In a normal photoreceptor, a whole series of reactions is needed to amplify the light signal," says Alan Bird of Moorfields Eye Hospital in London, UK.


Even if it does work, it is not clear how long the PSI centres will keep working, whether they will damage the nerve cells and whether there will be a problem with immune rejection. "It's like driving a device with a battery from another device hoping it will work," says Eberhart Zrenner at University Eye Hospital in Tübingen, Germany.


Retinal implants are likely to become available sooner, but they are limited by the number of electrodes that can be squeezed onto the array. Greenbaum thinks that treatment with PSI centres could provide better vision.


With both techniques, however, the visual processing that occurs between the photoreceptors and the ganglia would be lost. Other groups hope to restore the photoreceptors using stem cell implants or retinal transplants.




End of article.






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