The Patch

8:00 pm and I am rewarding myself. I just had a piece of chocolate and I am playing dance music on my iPad. This was the second day in a row I have felt as if I have actually accomplished something. Hallelujah. The to do list is starting to dwindle!

It won’t stay that way. Of course not. I know me. Besides, it is not good to become redundant. Meaning and purpose are like air. We need them to survive. Stay busy!

And on that note, I guess I should stop waxing philosophical and get to work here.

Lin sent me another article. As I alluded to on the last page, this one was about the development of a membrane to support the stem cell-derived RPEs. The research just keeps moving along!

It turns out this new development is coming out of Southern California. Specifically, the University of Southern California, the California Institute of Technology and the University of California at Santa Barbara.

Stop there a minute. University of California at Santa Barbara (UCSB)? Pete Coffey is at UCSB! The good Professor Coffey is co-director of their Molecular, Cellular, and Developmental Biology department. Gee, do you think there could be a connection? ? [Lin/Linda here: Professor Coffey is one of the researchers at Moorfields Eye Hospital in London who conducted the clinical trial that recently made the news with positive results of a similar trial conducted with 2 participants with wet AMD. He is also Director of the London Project to Cure Blindness. I found out that he splits his time 50-50 between University College London (UCL) and University of California Santa Barbara (UCSB). He isn’t directly involved in this study but does collaborate with the UCSB researchers.]

OK. Now it’s time to stop being a smart a** and tell you what they did; right? Right!

What they did was develop a “bioengineered implant consisting of stem cell-derived, mature, polarized retinal pigment epithelial cells in a single layer on an ultrathin synthetic parylene membrane”. Yikes. Let’s ‘unpack’ that as the saying goes.

Wikipedia gives an obscenely long and complicated explanation of bioengineering. You can look at it and figure it out if you wish. The definition in thefreedictionary.com was more simply “the application of engineering principles and technology to the field of biology, especially biomedicine, as in the development of prostheses, biomaterials, and medical devices and instruments.”

We have gone over stem cells quite extensively. We also mentioned that RPEs are polarized but I will go into that a little more deeply. In biology having polarity means the cell has distinct anterior and posterior parts. There is a ‘head’ and a ‘tail’. If they don’t line up right, they don’t work right.

Parylene is a polymer and is ‘green chemistry’. I refer you back to Wikipedia if you are interested in reading more. Social scientist here!

The purpose of putting the stem cell-derived RPEs on a membrane was to support them and and maintain their polarity. The patch was delivered to the back of the eye via the subretinal space (which we have talked about before) during an outpatient surgical procedure.

So how did they do? Apparently pretty well. Bear in mind it was only a phase 1/2a trial and there were only a few subjects, but the ‘patch’ seems to have integrated well and some of the people showed improvement in visual acuity.

For you on the west coast: they are enrolling subjects in six, different locations in California and Arizona. The clinical trial number is NCT02590692. If you are interested, get crackin’! Their numbers will be very small.

Next: Picturing AMD

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Eye Poop

Today was a “get your ‘stuff’ together” day. Every once in a while it gets so that if I don’t stop and take care of the business at hand, I will be having a screaming fit.

Like last evening for example! However, I have now gotten a haircut, gone grocery shopping and cleaned the living room, as well as having completed a few other tasks, like taking the recycling. Feeling a little more in control – I probably should not say that too loudly – and ready to tackle a page Lin suggested.

That page will be on – drum roll, please – eye poop! Okay, so that is not what they are really called. Most of the world call them drusen.

In a Harvard Health Publishing article that asks the questions: what are drusen and why do I have them, the author describes drusen as “deposits of extracellular waste”. You got it, eye poop.

In younger people, the sanitation department in eyes generally takes care of the eye poop. That ‘sanitation department’ is the retinal pigment epithelial cells aka RPEs. Yes, your RPEs are supposed to ingest eye poop. But you know what? Your RPEs are into recycling, too! They are discovering your eye is its own, little ecosystem. James Hurley at the University of Washington at Seattle and his team have discovered RPEs and the retinal cells are in this close relationship in which the wastes and byproducts of metabolism in one type of cell are the food another type of cell needs. Mess up in one part of the system and everything goes to Hades.

Why would the RPEs stop doing their recycling thing? No answers, just theories but one thing is for sure, age has something to do with it. Most people over 60 have at least a few piles of eye poop hanging around.

You know how it goes. Things don’t seem to work as well when we are older. Some messes pile up.

http://patient.info/health/age-related-macular-degeneration-leaflet

Eye poop becomes a problem when it starts wiggling in between the RPEs and the Bruch’s membrane. Bruch’s membrane is where the RPEs get the nutrients they need to feed the photoreceptors.

Think of it as a huge landslide standing between you and the grocery store. If you cannot get to the store, you go hungry and may die. If you die, those you are responsible for die too. Same with RPEs and photoreceptors.

Again, no one is exactly sure why some people get away with just a few, stray piles of eye poop and others have dozens. There is an underlying error or errors that have yet to be proven. The researchers are working on it.

The Harvard paper points out drusen aka eye poop do not cause AMD. They are just manifestations of the disease process.

Hope that was a help. Hope you understand things a little more thoroughly. Night!

Written March 18th, 2018

Next: Another Cautionary Tale

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Progress Daily

I really cannot win with this transportation business. Now they are on a string of late pick-ups and I am waltzing in 45 minutes after everyone else. Grrrrrrrrrr!

Oh well, can’t fix it. Time to start a page…..and as soon as I am into it, they will show up. Same concept as going to the bathroom in the restaurant to ‘make’ your meal arrive faster. Aha! Recognition! You have done that, too!

PRELUDE, the study, is NCT02659098. I checked and this is the same study I put my name in for last year. I just shot off a message to my research contact and asked her to make sure my ‘registration’ is still good. I am nothing if I am not persistent. Sad to say it is one of my better traits (oh no!)

There are actually two, main measurable outcomes they are interested in. There are the efficacy of the delivery system and best corrected acuity after administration of the stem cells. In the clinicaltrials.gov post they refer to the stem cells as CNTO 2476. In other literature they named the stem cells Palucorcel. I guess it is better than George (with apologies to the royal family. I have never liked the name George, although the little guy is a cutie!) Of course, Palucorcel does not exactly fall trippingly off the tongue.

Anyway, according to a one page write-up by Jessica Lynch, previous attempts to circumvent the vitreous and go in subretinally caused too many problems. They are, as I had been led to believe previously, trying to go around to the macula using the suprachoroidal space as their passage. (Anyone ever see Fantastic Voyage? I keep thinking how incredible it would be to jump in my microscopic submarine and motor through the suprachoroidal space!) After preclinical trials with mini pigs were successful, they launched into prime time with a phase 1 trial with people. As I said, they are now recruiting for phase 2. [Sue wrote about subretinal and suprachoroidal are in the previous page: Secret Passages in the Eyeball

Looking at the additional data on clinical trials.gov I discovered there are secondary outcomes for the study. They will be looking at quality of life and reading speed as well as whether the stem cell transplants slow or even stop the growth of the geographic atrophy. They are also looking at how many people convert to wet AMD. It sounds as if this study would be a long term commitment for the ‘lab rats’ chosen.

Going back to the Medscape article about phase 1, I discovered they had pretty good success threading through the space and the transplanted cells grew and started to function.

Cell placement was important. They used the microperimetry to figure out what retinal areas the subjects were using for eccentric viewing. Too close and that could be messed up. Cell placement other places was better.

Results? The subjects had some improvement in vision. That was SOME. Before you get too excited, remember this is RPE replacement. RPEs do not see. They support your photoreceptors. Some of the photoreceptors that are at death’s door may come back but the dead ones stay dead.

I did run off the journal write-up on phase 1 and I promise to tackle it and see if there were any other cool findings. Later. Right now I have laundry to sort. Maybe listen to an NCIS episode. It is now playing all the way through on my tablet! What can I say? It really is the little things.

Progress daily, guys. Progress daily. We will get there.

written October 17th, 2017 Continue reading “Progress Daily”

Eye Poop Reduction

Looking for information on therapies that slow the vision cycle. Got all sorts of things on slowing traffic for safer cycling.

While I am all for fewer car/bicycle accidents, that is not exactly what I had in mind!

Back to Wikipedia, I discovered the visual cycle is the process through which light is transformed into electrical signals. If you have a penchant for chemistry, I refer you to the Wikipedia article. Social scientist here! As far as I am concerned…then there is magic!

Part of this magic includes having three different types of cone cells that respond to three, different wavelengths of light. By taking stock of the strength and blending of the stimuli from these three, types of cone cells, we are able to see color! Cool! Although my guess would have been the primary colors, the colors they detect are actually red, blue and green. Why? Dunno. Magic.

But back on track, visual cycle…

Since the job of RPEs is not only to feed the photoreceptors but also to clean up after them, RPEs have to be able to tolerate a lot of…uh, poop. (Gee, maybe I am just a big RPE! I feel like I deal with that stuff all the time!) When there is too much poop for them to handle, we get, among other problems, drusen.

Janet Sparrow in Therapy for Macular Degeneration: Insight from Acne (catchy title?) said “it is the responsibility of the RPE to internalize the membranous debris discharged daily by the photoreceptor cell.” In other words, they eat eye poop. Unfortunately, some of the molecules in the poop are toxic (as if eating eye poop was not bad enough) and not at all good for the RPEs or surrounding cells.

The theory goes something like this: Less eye poop would make life easier for the RPEs. While we cannot get rid of all the eye poop – after all it is a byproduct of what we want: sight – maybe we can reduce the volume of how much poop we actually have to deal with. If we slow down the chemical processes involved in sight maybe we can produce less poop and thus see for a longer period of time.

They are checking out that theory right now. Foundation Fighting Blindness (FFB) advertised for subjects for a phase 2 (proof of concept) clinical trial of ACU-4429, a “visual cycle modulator”. For our purposes, read “eye poop reduction strategy”.

FFB also published a one page blurb about Fenretinide. Fenretinide has successfully completed phase 2 clinical trials and is on the way to phase 3. They are hopeful it will slow down the visual cycle in those with dry AMD. The slowing should lead to fewer lesions in dry AMD and fewer cases of wet AMD.

Oh, and that chemistry I referred to earlier? I might actually have to understand some of it. Oy. In the visual cycle there is a pigment-y sort of thing called 11-cis. Helping the light signal along its way to become sight causes a chemical change in the 11-cis. In order to get changed back to its original form so it can do its job again and not contribute to the eye poop problem, 11-cis needs help from several molecules, one of which is REP65. REP65. Remember that name. It may be an up-and comer.

written October 14th, 2017 Continue reading “Eye Poop Reduction”

Important Cells

You would think that after saying I was running out of ideas, I would have the good grace to actually run out of ideas and shut up. You should be so lucky!? [Lin/Linda: =I= should be so lucky! ::grin::]

A comment was made suggesting we may have fostered some misinformation. We have stressed the idea of retinal pigment epithelial (RPEs) cells supporting the photoreceptors in the macula so much we may have given some people the impression the RPEs are only under the macula. This is not true. RPEs are under all of the photoreceptors and support all vision, not just central vision.

Once again my very erudite source, Wikipedia (I did print out another article but it is long and involved and I can probably get three or four pages out of it. Do you really want that?) reports the RPE layer was first discovered back in the late 1700s, early 1800s. It was noted to be black in color in many animals but brown in humans. This is because this single layer of hexagonal shaped cells is chock full of – all together now! – pigment. The RPE layer wraps around the back of the eye and ends practically at the iris.

We have talked about a couple of the functions of the RPEs. They are there to feed and clean up after the prima donna photoreceptors – both central cones and more peripheral rods – that apparently cannot do things for themselves.

Something I had not heard of before but makes sense is RPEs, as the conduit from the bloodstream to the interior of the eye, are also the gatekeepers. RPEs are at least partially responsible for the immune privilege of the eye. Remember we talked about how the eye is such a great place to do stem cell experiments because the immune response is so weak? Part of that weakness is due to the great jobs the RPEs usually do. They block bad things entering our eyes from the rest of our system.

RPEs gather up scattered light to make images sharper. That also keeps the light from causing extra oxidative stress.

Simply put the visual cycle is the amount of time as well as all the steps it takes for pigment in the photoreceptors to be depleted and then build back up again. The RPEs do much to control this.

Lastly, the RPEs produce signalling molecules that ‘talk’ to different parts of the system. Lots of very important functions for a one-cell thick layer of cells.

Age-related macular degeneration is not the only condition that causes vision loss due to malfunctions involving the RPEs. A more common one you may heard of is retinitis pigmentosa (RP). Their losses start in the periphery and progress inwards. Those with RP go blind. That’s BLIND. Maybe we ARE the lucky ones.

Do I know why our deterioration generally stops at the macula? Nope, but I have it on good authority it usually does. Usually does not mean 100% guarantee. Just usually. It is the best that I can do.

written October 10th, 2017

Continue reading “Important Cells”

Reading Modern Retina

Never thought I would be skimming back issues of Modern Retina, but here I am! Let us get back to some of the science stuff.

Amyloid beta is a major component of plague found in the brains of those with Alzheimer’s. There has been some suspicion AMD and Alzheimer’s are related at a genetic level. A recent study completed by Cheryl Guttman Krader failed to show any positive effects of injecting an antibody that targets amyloid beta into the eyes of those of us with geographic atrophy.

For the time being this means this line of inquiry will be abandoned or re-worked. Proof of concept did not occur and these researchers might go on to investigate something else.

Why are negative findings good news? One less blind alley to investigate! Since we don’t know which ideas may bear fruit, they all have to be investigated. Eventually we get to only the ones that have the most promise. Scientific method.

And another reason I think this finding is good news? It sort of suggests the Alzheimer’s and AMD connection may not be so cut and dry. Phew!

Here is another failure in proof of concept. Aflibercept is called Eylea when it is used as an inhibitor of vascular endothelial growth factor (VEGF – read “one of the things that makes the extra veins grow in AMD”). Michelle Dalton tried implanting stem cells in the eyes of patients who had been getting Aflibercept. She hoped the stem cell would produce the natural vascular endothelial growth factor and make the shots unneeded.

Unfortunately, many more patients than she had hoped required rescue doses of the drug. However, she also had people who kept the stem cells alive and these imported new stem cells did produce some of the Anti-VEGF molecule. Quantities were just too far below a therapeutic dose.

While this may be a failed experiment on the face of things, it is not all bad. Knowing there was some production of the desired molecules means this procedure may be very helpful once they figure out why it worked the little bit it did. Magnifying that effect may lead to fewer injections.

Last one, David S. Boyer wrote a review on multiple strategies being investigated for treating dry AMD. While many protective strategies for our photoreceptors and RPEs have failed, one they are still looking at with interest is brimonidine, brand name Allergen. Allergen is once again an intravitreally administered drug. (That is needle in the eye. We appear to be destined to join our wet AMD friends in that fate!) Coming out of phase 1 trials, brimonidine looks good. Next for it is phase 2, proof of concept. Will it perform as hoped?

Glatiramer acetate is looking good for reducing drusen. Glatiramer is used to treat multiple sclerosis, a disease in which the immune system wears away at the covering on the nerves. The theory is that glatiramer acts as a decoy to mitigate the autoimmune reaction. This treatment is based on the idea AMD really is an autoimmune disease.

There has been some evidence glatiramer reduces drusen, but Dr. Boyer warned us drusen can become fewer on their own. Drusen regression.

And that is a topic for another page.

written June 26th, 2017

Continue reading “Reading Modern Retina”

BIG News!

Woke up with a start at 2 am last night. Probably several things.

First thing that happened was a call from one of my contracts. She had called my third place of employment to schedule an evaluation and was told I did not work there anymore!

News to me! Now, I don’t get there a lot but the plan was for me to go and do a case or two when called. Maybe something like once every six weeks or so. I was never told I was being fired!

Of course it turns out someone got something wrong but it did get me to thinking. Once again, how does one graciously bow out or – hopefully equally graciously – be shown the door? Inquiring minds.

The second thing that has me a little anxious is my big ‘field trip’ tomorrow. I am going to do some sightseeing on Manhattan with an acquaintance from school. First time that far away from home without my husband since my sight loss. I know it can be done, but it is still a little scary.

Third thing: I saw Regillo yesterday. My eyes are getting worse slowly. (I am not so sure about the slowly part!) He confirmed scotomata (aka blind spots) get darker but did not necessarily say they go black. He said that he would not expect a central vision loss to cover 60 degrees of arc. That wide a loss would be ‘extreme’. Those two answers at least get us slightly closer to settling two of my burning questions from this Spring.

The big news, though, is he wants to try me on lampalizumab next winter. It appears the phase 3 clinicals are going to wind down by the end of the year and phase 4 trials will be starting.

People, the numbers of subjects in phase 4 trials is BIG. HUGE! Phase 4 trials take place after the FDA approved the marketing of a new drug. The drug is made available to the public through local physicians. They look for effects and side effects in diverse populations.

What this means for you is simply this: the first actual TREATMENT for geographic atrophy may only be six months away! This is the first breakthrough!

Lampalizumab is an injectible drug. It has been proven to slow the progression of geographic atrophy and to “reduce the area of geographic atrophy” by 20%. Dosing occurs monthly or every six weeks.

Will I do it? Probably. I really believe stem cell replacement of RPEs is the way for me to go, but it is taking forever and I don’t have time for forever. Lampalizumab can be administered locally and would avoid lots of trips to Philly. I don’t like the idea of intravenous injections but I don’t like the idea of a vitrectomy either! A 20% decrease in disease progression might win me enough time (and macula!) to have a more successful intervention later.

If you have dry AMD and geographic atrophy, it might be worth your while to broach the subject of lampalizumab with your retinologist. Let him know you are interested. This could just be the start of something big for all of us.?

Continue reading “BIG News!”

Yesterday’s News

Good morning! Lin just shared a video clip from something that looked like a local TV, health program. The clip was on geographic atrophy. That is GA to those in the know.

I have no problem with information being shared with the public. In fact, I think it is a good thing. The more exposure we get and the more noise we make I am hoping two things will happen. One would be law makers (read the deep pockets of government) will be more aware and sympathetic to our plight. (They might also come to realize it is going to cost BIG bucks to care for us!) The other will be people who have AMD will become more knowledgeable and go for help and support.

There are some drawbacks to these little TV presentations, though. For one, they are a bit behind the curve when it comes to breaking new news. The show talked about a fantastic, recent development that would help people with GA.

Fantastic? OK. Helpful? Yep. Recent? Only if you consider research published in 2013 to be recent. So shoot me. I am an information snob. That information was just too yesterday’s news for me.

I also think they present half information. If you listen to the clip you will hear the expert talk about a ‘subset’ of patients who cannot be helped with current treatments. Not to put too fine a point on this – and look out because I can feel myself getting ready to rant! – but, honey, the group that can be helped with current treatments is the subset! 15% of AMD patients ‘go wet’. The 85% of us who are left are not the subset! (Told you I was going to rant!)

In the clip there is the implication that replacing RPEs will restore sight. We have talked about this a dozen times before. In GA the photoreceptors are dead. There is no sight without photoreceptors. The RPEs are support cells for the photoreceptors. They do not do any of the ‘seeing’.

But my big complaint about this clip? The expert says your world ‘ends’ when you develop GA!!! (Now I am really revving up. Head for the storm cellar!)

With every significant loss, there is a time of dismay and distress. That does not mean the end of your world! Everyone of us here is made of tougher stuff than you could ever have believed. Maybe you have never been tested before, but the steel is there.

Today I taught my class. I attended a staff meeting and saw two clients. Then I came home, walked the dog and made a meal. I am now writing this page. After that I have a psych report to write. Then maybe some down time ‘reading’ a BARD book.

Tomorrow I work, walk with a friend and go to my yoga class. I am making plans to go into New York City with a co-worker next month. The list goes on.

In short, if my world ended a year and a half ago, nobody bothered to tell me about it! I am still going pretty much full tilt!

So, bottom line? I guess it would be listen to the stuff in the media but remember it might not be accurate or current. Once again, caveat emptor. Best sources still remain published research. If you cannot read it or cannot understand it, ask Lin or me to look at it and we can tell you we don’t understand it either!

And about that end of the world business? Don’t believe everything you hear! GA is not a walk in the park. However, if you want to, you can still do that and dozens of other things as well.

Continue reading “Yesterday’s News”

Sisters Are Doin’ It For Themselves

I have paid a lot of attention to the male movers and shakers in vision research. Perhaps it is time to note the contributes of the women. Recently I have come upon short articles about the research of two.

Sally Temple, SUNY-Albany, and her colleagues recently published a paper on how nicotinamide can suppress the progression of AMD. Nicotinamide is a vitamin B3 derivative.

Dr. Temple took pluripotent cells, that is stem cells, from people who had AMD and those who did not. She manipulated the stem cells to become retinal pigmentation epithelial cells and grew them in her lab.

One of the first things Temple and her team noted was the cells from the AMD people acted differently from the RPEs grown from healthy subjects’ cells. The cells from people with AMD produced different chemicals. The chemicals were the same ones that figure in the production of drusen and contribute to inflammation.

These were RPEs growing on a culture medium in a glass dish. There was nothing else to contribute to the formation of the chemicals. The chemicals had to be coming from the RPEs. And, with no other possible influences, the cause for the production of these chemicals pretty much had to be genetic.

The fault, dear readers, is not in ourselves but in our genes. One more tally in the genes are destiny column.

But the good news is, when they squirted (or whatever) nicotinamide on the offending RPEs, things improved. Chemicals that are responsible for the bad things were less and the RPEs survived longer.

Perhaps if we find a way to get nicotinamide directly into eyes, we will get the same results in vivo as in vitro. Worth a try.

Masayo Takahashi is a Japanese researcher. Takahashi has been experimenting using pluripotent cells taken from the same people they are going back into. No embryonic cells required.

There is excitement about this new procedure not only because of ethical issues. There are indications this procedure will be cheaper and faster to implement. In additional, they are thinking people can ‘bank’ their stem cells. These can be used either for ‘repairs’ in the original cell ‘owner’ or they can be given to other people who are immune matched. (Sort of like blood type matching. Don’t want the body getting up in arms over the ‘invading’ materials.)

Bottom line is the ladies are out there rocking it just like the men. They continue to come up with great new findings and each one takes us a little bit closer to effective treatments and maybe – just maybe – even a cure.

To copy Lin’s use of old song titles, “sisters are doing’ it for themselves”. And they are doing it for us, too! Continue reading “Sisters Are Doin’ It For Themselves”

Always Learning More

Hey, there! I think I have found a good article on macular degeneration, our favorite but somewhat distasteful topic. The article is in Webvision and is entitled Age-Related Macular Degeneration. Another catchy title. The main author is Hageman.

Did you know the name up until around 1990 was ‘senile macular degeneration’? Makes it sound like our eyes have lost some of their mental faculties. Glad that was changed!

Also discovered the fovea is the center of the macula. It contains the highest concentration of cone photoreceptors and is the only region of the retina that can attain 20/20 vision.

I think when my optometrist said I had such an abrupt vision loss because the deterioration had reached the center of my macula she was talking about the loss of my fovea. That means 20/20 vision is no longer possible for me. Even if I use prisms or eventually get that eye max mono thingee, things will not be ‘perfect’. [Lin/Linda: she means the EyeMax Mono lens implant.]

This article says macular vision is 10% of vision! Estimates of degrees of arc of potential loss seem to be getting better, but don’t get too excited. Remember we are talking my interpretation of things I read. It is guess-work. I know nothing.

Although I used to think hard drusen sound more ominous than soft ones, it is actually the other way around. Hard drusen are smaller and soft ones are larger. If they are looking in your eyes and mention soft drusen, you have more of a problem than if they see hard drusen.

I thought that all dry AMD would progress to GA (geographic atrophy) if the person lived that long. This article says only 10 to 15% of dry AMD patients progress rapidly enough to ‘achieve’ GA. Interesting.

That means my visual state is something many of you will not have to experience. That is a good thing! And FYI? I am functional so you can remain functional as well.

For you ‘wet’ folks, the article once again cautions you to stay on top of things and get your shots. Left to its own devices wet AMD progresses to a cicatrical stage. Cicatrix is a fancy word related to scars and scarring. Disciform scars occur when fibrous tissues develop in Bruch’s membrane between the RPEs and the retina. Scarring is, needless to say, not good and can result in severe vision loss. Bottom line for this paragraph is: do not allow bleeds to happen to you!

Closing in on my 500 words and I still have pages to read in this article. I think I will close this page, read some more and start another.

And FYI, I emailed by doctor. And – while he also believes the increased density/opacity of my blind spot is related to expected disease progression – I am going in for a vision screen in two days. Perceivable changes in your vision? I expect you to call, too. Check it out.

written April 25th, 2017

Continue reading “Always Learning More”

Good Thought, Bad Thought

Back again in the same day. You do know I am ridiculously hard to get rid of; don’t you??

This is the page I was going to write before my ZoomText, inelegantly put, took a dump. Now I will write it.

I went to see my local retinologist Monday. Great guy. He is good. His kids are good. I feel I see him enough I get to inquire about the boys.

I also feel like I am becoming ‘friends’ with my tomography tech. We chat. I asked about the enhanced depth tomography. He had the capability with his machine and since it would not cost any extra, he ran it on me. The pictures were pretty. I saw my optic nerve and my ‘divot’, geographic atrophy, but did not have the training to see much else.

The tomography tech pointed out two veins in my choroid. They were old veins, not new ones. It is sort of bizarre to realize how relatively deep the hole is in my macula, but that is a part of the definition of geographic atrophy; the damage is choroid deep.

Neither my local retinologist nor I believe I will convert to wet AMD. He has put me back to twice yearly for my check-ups. It was my understanding, and my retinologist confirmed, that wet developed as an adaptation (sort of) to the dry form of AMD.

The way I understand it, when the RPEs and the photoreceptors are not getting enough oxygen and nutrients they send out the SOS . They need supplies! They are starving! The body responds by establishing new supply lines in the form of new blood vessels. The only problem is these vessels are inferior. They break and the bleed. Problem not solved. The fix does not work so well.

I got the impression I am back to twice yearly visits – and he does not think I am a candidate for wet AMD – because I don’t have a lot of macula left. Now he did not say that. It was an impression but I am usually pretty good at those. I don’t think there is much for my body to try to save anymore.

Good thought and bad thought. Or actually bad thought and good thought. Bad thought that I may have reached this level so quickly. Good thought: could the slide be over? Will I soon stop losing vision?

Now, cheating my sweet little patootie off and using eccentric viewing and guess work to the max, my vision tests as 20/50. Am I really 20/50? No, but I cheat well. And they know I cheat, by the way. I tell them every time.

If I can cheat and test at 20/50, that means I have decent functional vision. I can do a lot with that. Not so bad.

So why all the horror pictures of visual fields that are 90% bleach white with decent vision around the edge? If this is a ‘central vision loss’ problem, what is the definition of central vision?

No clue, but Lin and I are on the hunt. Let ya know. Continue reading “Good Thought, Bad Thought”

Kids and Zombies

This page is going to be another mixed up affair. I don’t have a full page on either of a couple of totally unrelated topics. Hope you don’t mind if I cobble them together.

First thought: I have talked about loving my big people and have not said anything about my little people. Let me correct that. I love my kids!

We may have an exceptionally tolerant and loving group of kids at our school, but I don’t think so. I think kids are just naturally adaptable and loving. It is the nature of the beast.

Anyway, my kids are wonderful. They take my telescopic glasses and CCTV in stride and think they are cool. My disability? Yeah, she doesn’t see well. What else is new? So what? Can we move on now?

The other day I was waiting for my ride, sitting in the office with all my gear. A little girl about seven was waiting for her mother. The little girl asked about my stuff and I first told her I have an ‘old lady’ eye disease. I think I am going to take this little darling home with me! Her response was “you are not an old lady!”

Then I told her I used the equipment to help me so I could continue to work with the kids at school just like I like. Her response? “Thank you”. OMG. I love my kids.

Second topic: Back to stem cells. Lin gave me an investment article. It was dated July, 2016. Mark Collins writing for marketexclusive.com suggested people invest in….drum roll, please….Astellas Pharma!

For those of you who just walked in, this is the company sponsoring one of the stem cell trials I am signed up for. I am thrilled to hear that this company is being touted as a good investment opportunity. It means the company is seen as a moneymaker. And how are they going to make money? By bringing the stem cell treatment to market, that is how!

Collins cautions this is a somewhat long-term investment. It may be two or three years until the product is brought to market, but the financial analysts are very positive about its future.

I am signed up for phase 2 clinical trials. If Collins is accurate in saying they should come to market by 2020, phases 2, 3 and 4 will have to come about in pretty short order. Good.

One more quick note: please remember RPE stem cells may stabilize vision. That means things won’t get worse but they won’t get better either. There is a bigger maybe for restoring some vision. Subjects in phase 1 got a few letters (not lines) on the eye chart back. RPE stem cells do not cure AMD.

Geographic atrophy, aka advanced dry AMD, means I have dead photoreceptors. Dead is dead. No zombies are produced in this procedure. That means it is not a cure. They are working on a cure but it is not expected for at least 10 years.

[For a review of what RPEs and photoreceptors do, see Sue’s page The Science Stuff.]

As always, I often do not know what I am talking about, so please check the stock tip with your broker….but if you make a billion dollars? Remember me! ? Continue reading “Kids and Zombies”

SOS

J.R.R. Tolkien said once that “false hopes are more dangerous than fears.”

Every once in a while Lin and I hear someone make a claim about AMD that we know is not true. Then someone picks up on the claim, believes a foolproof treatment or cure has been found and they have been saved from blindness. This is only to have their hopes dashed a day or two later when the truth comes out. This can be heartbreaking to watch, let alone experience.

Right now, to our best knowledge, there is no cure or available treatment for dry AMD. There are a number of treatments being tested. Even the treatments most advanced in the process are several years away from being available to the general public.

The SOS has been sent. The cavalry is coming but they are still a very long ways away. It is up to us to hold out until then.

When I talk about medical treatments, I am talking only about drugs that will slow the deterioration process. To my knowledge there are no drugs that will regrow RPEs and/or photoreceptors. The drugs will not restore sight. If you have lost your photoreceptors, at this point in time you have lost your sight.

Stem cell replacement at present is for RPEs only. Remember RPEs are only servant cells. They take care of the photoreceptors. The pizza delivery guy may help to keep the neurosurgeon alive but we would not expect him to do brain surgery. Same concept. The RPEs will feed the photoreceptors but they won’t turn light into sight. The best we can hope for is for some of the photoreceptors that are at death’s door to be revived and start working again.

Dead photoreceptors are just that, dead photoreceptors. I have geographic atrophy. Photoreceptors that should be in that area are dead and gone. There is currently no way to get them back. The last I heard they were able to grow photoreceptors but they had been unsuccessful in having them connect with the rest of the nervous system. You have a cell phone in a deadzone. Your phone works great but the signal goes nowhere.

Am I saying have no hope? Hell, no. I live on hope. Just have realistic hope. Treatment is coming. Cures are coming. Just don’t expect them next Tuesday!

Why do people get so hung up by these crazy claims? First of all, they are desperate. Any port in a storm. Beyond that I am not sure. I wasn’t able to find a lot on the mechanisms behind false hope. Maybe it is better to feel better for a little while even if you are destroyed later. Sort of like substance abuse. It felt good at the time.

We try not to deal in rumors, just facts. If we say something you do not think is true, challenge us. If you read or hear something different from what you hear here, alert us to it and we will research it. Better yet, anybody capable of web research might volunteer to help us. There is a lot of information out there.

In the meantime, keep the faith but don’t go crazy. We are not there yet.

Continue reading “SOS”

Video: What is Macular Degeneration–the Science Stuff

A Perfect Storm

January 31, 2016 was a breathtakingly beautiful Winter day. I know it was January 31 because I still have the ski tag on my jacket.

That day I drove to Wilkes-Barre and had lunch with a friend. I was able to read the menu. I was able to navigate the roads.

I left lunch and went to a local ski area where I had a glorious, three-hour session of skiing. The sky was bright blue with not a cloud to be seen. The snow was a glittering white. The air was mild but not mild enough to make ‘spring conditions’ also known as slop.

I wore my sunglasses constantly. Of course I wore my sunglasses. I knew I had macular degeneration and that’s part of the drill. My sunglasses were red and matched my jacket. Even we old ladies with eye problems like to look good on the slopes.

Of course I wore my sunglasses. I knew I had macular degeneration and that’s part of the drill.

Later, my husband insisted it was photostress that destroyed my macula. He believed the day on the slopes and the reflection on the snow was just too much for my eyes to handle. My optometrist and ophthalmologist did not agree but there is that lingering doubt.

A quick detour here to talk about photostress. Photostress is, exactly as the name suggests, the stress that light puts on your eyes. When the photoreceptors make ‘light into sight’, they deplete a chemical, basically a pigment, that has been fed to them by the RPEs. Remember those Servant cells that take care of the photoreceptors? To my understanding, photostress happens when the light is eating up so much pigment that the RPEs cannot keep up replacing it.

If you have ever gone ‘snowblind’ you understand what I’m talking about (although snowblindness is caused by something different).

In the past I have had trouble with photostress. I walked from the car to the building housing a yoga festival. I had forgotten my sunglasses but did not think much of it. I stood in the lobby for five minutes–blind.

There is a photostress test in which they purposely make you go blind and see how long it takes you to recover. It would appear that recovery time is the key variable here.

Recovery time is the key to knowing how serious the photostress is.

If you’re reading this website just because you have nothing better to do or out of curiosity, if you do not yet have a diagnosis of retinal disease and you become blind after coming in from bright light with long periods of recovery, get thyself to a reputable eye doctor. It is very possible you have the beginnings of a retinal disease. That’s the public service announcement.

If you become blind after coming in from bright light with long periods of recovery, get thyself to a reputable doctor.

Written February 2016. Reviewed September 2018.

Continue reading “A Perfect Storm”

The Man Behind The Curtain: The Wizard of Wills

For a rock star of retinas, Regillo, was not all that imposing. I finally got to see the man after multiple tests by multiple technicians. Towards the end of the gauntlet, I asked the girl if everyone went through so many tests. She confided in me that many people do not get as far as I got. That was certainly encouraging. My inner voice had been telling me I was on the right track. The stars seem to be aligned. However, this was the first outside confirmation that I had chosen a good path.

I had chosen a good path. The stars seem to be aligned.

When the good doctor came into the room, I was studying the scans of my left eye–not quite sure why, but he appeared to be amused. Perhaps this was highly unusual behavior in a patient with Age-Related Macular Degeneration.

Regillo proceeded to challenge me to tell him what I saw. So I told him. The lower area was Bruch’s membrane. This membrane is the connection to the proverbial greater world. It brings nutrients to the RPEs and takes away the garbage. The level above that contained the RPEs. It also contained yellowish piles of eye poop more appropriately known as drusen. Level above that were the photoreceptors. The divot in the top was geographic atrophy and the reason I was there.I might have impressed him. After all, I am more than just an impaired eyeball.

I am more than just an impaired eyeball.

Strange, staccato, conversation followed. I told him I wanted to read the article on the phase 1 results when it came out. It was out and he gave me the citation. I told him I had every intention of being in phase 2. The conversation was a bit of a tennis match. At times we are even finishing each other sentences. I felt as if we were definitely on the same page.

Also, talking to the doctor I felt as if we were in a cat & mouse game and I was the mouse. He seemed overly interested. No, not that way, I felt like I was prey but in a professional, scientific way. It was like he had found a live one. After reading the phase 1 results that were published in Lancet last winter, I figured out why. The mean age of the cohort for the phase 1 study was 77 years of age. The team was planning on doing a 15 year longitudinal follow-up on the study. There was now no confusion in my head as to why Regillo was looking at me as if I were a live one. Hell, in 15 years, with subjects like that, I was going to be the only live one!

The mean age in the phase 1 study was 77 years of age. That means in the 15 years of the study, I was going to be the only live one!

Written February 2016. Reviewed September 2018.

Continue reading “The Man Behind The Curtain: The Wizard of Wills”

Resources

June 2023 There’s an announcement that since Sue has not written any new journal pages for some time, the site has been archived until we can decide if the work necessary to make sure all information is accurate and up-to-date can be made. In the meantime, you’ll get some pages ‘not found’ or ‘private’ until that decision has been made. The emphasis for several years has been on the Facebook group.

2/14/2022 Because of the rapid and constant growth of our Facebook group, I cannot keep this list updated. I have a large amount of information available in the Facebook group in Guides which are like chapters in a book or lessons in a course. Plus, in 3 years, the amount of information in the posts and comments is quite substantial. I recommend that you join us there where you can get the information and the support to help you in your journey. Thanks for understanding. Hope to see you there! Lin/Linda…

I’ve added some pages from that group that might be of interest to you.

Frequently Asked Questions

Click here for the list of Frequently Asked Questions from our Facebook group.

AREDS2-based Supplements

There are several pages on the site that explain what AREDS2 means and who the AREDS2-based products are for. Click here to go to a list of articles.

AREDS2-based Supplements With 0 or 25mg of Zinc

Click here for the list.

Navigating

There are a lot of links here. I’ve set up this page so that when you click on a link (words that are underlined & in blue or green), a NEW tab will open in your browser and this page STAYS WHERE IT IS. When you are done with the new page you opened, just close it. You do NOT need to use the back option. If you click on a link and the new page replaces this one, I’VE MADE A MISTAKE so please let me know by sending me an email at light2sight5153@gmail.com. Let me know exactly which link or links do not open a new tab or window.

Errors: If you click on a link and you get a ‘page not found’ error, please let me know by sending me an email at light2sight5153@gmail.com. Let me know exactly which link or links do not open a new tab or window.

Additions: If you have a link you’d like to add, please email at light2sight5153@gmail.com.

Topics-click below to move to a topic

Links We Like
See what vision is like at the various stages of AMD
What is AMD?
Glossary
Websites devoted to AMD and Other Forms of Macular Degeneratin
Websites containing information about AMD and Other Forms of Macular Degeneration
Support groups
Where to find services
Books & reading materials
Videos
Personal stories of living with AMD
Online newsletters
What is Stargardt’s Disease?
Science Stuff
Symptoms
Risk factors
Treatments
Research/clinical trials
- How can I become part of a clinical trial?
Coping with vision loss
Self-maintenance/ self-care
More to come…

Links We Like

Click here for a GREAT resource where you answer some simple questions and you get a customized guide based on your responses
Click here for a great glossary
Click here for Low Vision Resources: A List of Lists (such as 8 ways to slow AMD, 15 tips for family and friends, etc)
Videos
- Click here for several videos
- Click here for the UK Macular Society’s Say Hello to Mac
- Click here for one that uses illustrations and animation (explains how wet AMD progresses and how the injections work)
Click here for a description of dry vs. wet AMD (we are not recommending any products in this article)
Click here for an article about depression after diagnosis
Click here for a very comprehensive page about wet AMD
Click here for a very comprehensive page about dry AMD
Click here for a FAQ (Frequently Asked Questions) that answers a long list of questions such as ‘will resting help my eyes?’, ‘Can I see for myself if my retina or macula shows any signs of damage before I have symptoms?’, ‘why don’t new eye glasses help?’, ‘what is meant by degeneration?’, ‘is a macular hole the same as macular degeneration’, ‘I have had dry MD for years. Does this mean I’m going to get wet MD too?’, ‘No one else in my family has MD. Why did I get it?’, ‘can drusen be treated?’, ‘I have changes on the Amsler Grid, does this mean I have MD’, ‘I have Wet MD but my Doctor says there is nothing he can do or no treatment available. Why is this?’
Click here for a short introduction to stems cells, what they are and how they can be used.

See what vision is like at the various stages of AMD

Click here to find ways to see simulations of what vision loss due to AMD is like at various stages.

Next: Picturing AMD

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Next: Another Cautionary Tale

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I’ve added some pages from that group that might be of interest to you.

Frequently Asked Questions

AREDS2-based Supplements

AREDS2-based Supplements With 0 or 25mg of Zinc

Navigating

Topics-click below to move to a topic

Links We Like

See what vision is like at the various stages of AMD

Glossary

Websites devoted to AMD and Other Forms of Macular Degeneration

Websites containing information about AMD and Other Forms of Macular Degeneration

Support

Message Boards including ones from

By postal mail

Start Your Own

On the phone/telesupport

Where to find services

Resources for Students

Books and reading materials

Specific Titles

Sources of Books

Videos

Personal stories of living with AMD

Online newsletters

What is AMD?

Wet Form

Dry Form

How fast does AMD progress?

What is Stargardt’s Disease?

The Science Stuff

Role of RPEs

Geographic Atrophy

Symptoms

Charles Bonnet Syndrome/Visual hallucinations

Other problems with vision & AMD

Risk factors

Age

Diet/nutrition (working on this section)

Race

Gender

Uncontrolled high blood pressure

Uncontrolled high cholesterol

Smoking

Blue Light

Eye Color

Aspirin & other medications

Other possible causes

Connection between AMD and Alzheimer’s Disease

Treatments

Injections for Wet AMD

Telescopic implants

Are there new treatments in the pipeline?

Vitamins (see Self Maintenance/Self Care section below)

Research/Clinical trials

How can I become a part of a clinical trial?

Gene Therapy

Bionic Eye/Retinal Implants

Nutritional Supplements

Stem Cells

Coping with low vision

Low Vision Aids

Wearable Technology