We can't say how long the 'verge' is. Certainly years. But is it years-years or decades-years? Quite possibly sooner than many might have guessed just a few years ago. I like to be cautious about predicting breakthroughs that have not happened yet, but the results reported a few days ago at a major conference seem to have solved or significantly advanced solving some of the key problems in using stem cells to grown eye tissue.
There had been a lot of promising news over the last few years, and one of the most astonishing finds was reported from Japan just a few days ago at the annual meeting of the International Society for Stem Cell Research in Yokohama, Japan. Research Yoskiki Sasai has produced a proto eye from stem cells. This is different than previous stem cell results in three very important ways:
1) This is a three dimensional structure, mirroring normal eye structure, unlike earlier stem cell work which has produced a much less useful two dimensional structure;
2) The lab-grown biological structure is anatomically complete having both rods and cones in proto-form. Previous work only produced usable rods. This structure would, if it worked, produce an "eye" or a "retina" (or some transplantable thing) that would see color and see well.
3) Stem cell produced products seem to have latent stem cells embedded in them, often, which is one of the risk factors for cancer as an unintended side effect. According to the report provided a few days ago, this method should not have that problem.
Also of interest, the researchers have developed a way of packaging the grown retinal tissue for shipment and storage.
We should be impressed and we should be thankful that the Japanese have continued to fund and carry out research that was illegal in the US for so long. Had this work been funded at the levels that US based research tends to be funded, we'd probably have packaged up retina replacements ready to go in eye clinics by now. Depending on how politics works out in the US over the next few years, this produce will probably not be available here anyway. Retinal transplants will probably only be done overseas in countries without Republicans.
There is much more to the story than this, having to do with findings about how cells differentiate, which perhaps we can cover another time. Read all about it here in a reproduction of an article from Nature. The original report is cited below.
Main source: Cyranoski, David. 2012. Biologists grow human-eye precursor from stem cells: Achievement raises hopes for optic repair in the clinic. Nature. 15 June 2012.
I would say no, at least not based on this research.
The most common retinal problem is diabetic retinopathy. It, and virtually all of the other retinal disorders are secondary to systemic metabolic disorders and are characterized by vascular remodeling which leads to retinal damage and failure.
Putting a brand-new perfect eye in an organism with a systemic metabolic disorder, will lead to vascular remodeling and retina failure.
What causes the vascular remodeling that results in neuropathy is disruptions in nitric oxide signaling. Unless the nitric oxide signaling is fixed, replacing damaged eyes with new eyes grown from stem cells will not be a long term solution.
In reference to that, yes. I was thinking of the less common but very diverse retinal degenerative diseases such as retinitis pigmentosa, macular degeneration, Usher syndrome, Stargardt disease, Best disease, choroideremia, retinoschisis, Leber congenital amaurosis, Bardet-Biedl syndrome, cone and/or rod dystrophies, achromatopsia, and Refsum disease, some of which have been treated successfully with so far fairly half baked implant and stem cell treatments. None of those derive from systemic disease, I think.
I've altered the title of the post to make it reflect that distinction.
Having said that, if this method of grown eye-parts is very easy and the surgury is reasonably easy perhaps it would work for systemic disease with the idea of replacing the things every five years or so. Or is the process of damage quicker than that?
I am pretty sure that macular degeneration is secondary to low nitric oxide levels. The characteristic vascular changes (tortuous vessels and nicking) can be explained through a low NO mechanism. Hemoglobin is the sink for NO, and low NO also causes vessel regression via low NO induced apoptosis. This is how the vascular geometry becomes coupled to the flow, as in a stream meander. Red blood cells are denser than plasma, so in curved flow, the red blood cells are accelerated to the outside of the curve where they are closer to the vessel wall and so that side of the vessel sees a lower NO level so it regresses producing the characteristic tortuous vessels.
I suspect that low NO is a final common pathway in many of these retinal disorders. There may be a genetic “cause”, but the retinopathy is mediated through a low NO mechanism (which is a common stress response) which is why they all look the same (tortuous vessels and nicking).
If you did fix the genetic "cause" in the stem cells you grew the replacement from, it might fix the genetic based retinal disorders, and yes, that won't be done in the US if Republicans stay in control.
It would be interesting to link a faulty genetic product to low NO levels in the blood; wouldn't there be other outcomes of low NO such as cardiovascular diseases in such cases? Age-relaeted macular degneration is linked to cardiovascular disease. Can NO explain the formatio of Bruch's membrane in dry AMD? The possible link to wet AMD might really be there, the disease looks a lot like what you describe.
btw a suspect gene is CFH (complement factor H)
Not knowing what Bruch's membrane is, I looked it up, and I would say yes, via several mechanisms. Low NO lowers the ATP level which turns down autophagy allowing bad stuff to accumulate. This is a "feature", you don't want to waste ATP on getting rid of garbage while you are running from a bear, so the low NO of the fight-or-flight state turn those things down and eventually off.
I have written up a lot of the details of how NO regulates vascular stuff.
In looking at pubmed, there are specific markers for low NO in Bruch's membrane.
Nitrated proteins are a sign of insufficient NO. Nitrotyrosine comes from peroxynitrite, peroxynitrite forms from superoxide and NO, they react at diffusion limited kinetics. Peroxynitrite damage only occurs when there are near equimolar production of NO and superoxide. If either one is in excess (by 2x or so), there is no production of nitrated proteins.
There are pathways by which CNVs lower the NO level. I think that is the major mechanism by which CNVs cause various disorders. Genes that raise NO levels cause autism when they are deleted, genes that lower NO levels cause autism when they are duplicated.
I have sent you a poster I presented at the Autism Consortium on this.
Sorry for the moderation, it's the links. I just increased that to 4 before moderation. Spam does not use that many links these days.
I wonder if the people researching this are looking at NO.
They are not looking at NO. NO is considered to be too complicated and involved in too many things to be feasible to do research on. There are no ways of increasing NO levels, other than my bacteria pretty much, but I haven't been able to get enough attention and funding to get the data to "prove" that my bacteria are important.
The problem is that people who are studying other things want/need their stuff to be "the most important thing ever", to get funding and kudos. They have to (at least unconsciously) denigrate that which they are not working on and which they don't understand.
It is very much like the anti-sceptics who don't know the field, but argue against it anyway based on non-fact-based arguments.