Cataracts and AMD

Hunting around for a good topic and AMD and cataracts popped up in the search. Daddy had both and I would suspect some of you have both, too. Is there a relationship between AMD and cataracts? If so, what is it?

Turns out those are excellent questions. The experts are falling on different sides of the fence as to whether or not there may be a relationship between them.

Back in the earlier years of this century (2002) the good folks in Wisconsin, the Beaver Dam Eye Study people, again looked at their subjects after ten years had passed. Statistically, there was an indication that cataracts alone are associated with early AMD. There was also a statistical correlation between cataract surgery and late AMD.

Once again, we are looking at correlation. Correlation does not assume causality. Want a giggle over crazy correlations? Go to the website Spurious Correlations for some fun graphs. You will quickly see how just because things correlate they may not cause one another.

Anyway, like I said, they are still casting around to try to get some definitive answers on this question. The Chesapeake Watermen Study found a correlation between having cataracts and AMD but the Framingham Eye Study and some early Blue Mountain work did not.

But what about a correlation between cataract surgery and late AMD? Beaver Dam found cataract surgery before baseline (initially study measures) was associated with increased risk of late AMD. In fact, eyes that had cataract surgery were four times as likely to develop geographic atrophy and three times as likely to develop wet AMD! Holy freakin’ moley! How do you like that for being between a rock and a hard place?

Of course, like, I said, there is no certainty in any of this yet. In AREDS Report 25, Chew et al reported no correlation between cataract surgery and ARM. Hard to know who to believe.

So, what to do? No one is saying to go blind with cataract now rather than wait and go blind with AMD later. Do what you have to do to see.

FYI Blue Mountain, fortunately or unfortunately, flipped over to the significant correlation camp in reviewing results of a 2006 study. While that may not be great news for those with cataracts, Blue Mountain also shared yet another point they agree on with Beaver Dam. They discovered nonphakic eyes had a three times greater risk of developing late stage AMD as opposed to phakic eyes.

I know. I know. Don’t get your panties in a bunch.  Here is the explanation: in phakic cataract surgery, there is a small incision made in the front of the eye and the artificial lens is implanted. The natural lens is not removed. In nonphakic cataract surgery, the lens is removed.

Talk to your doctor, but as it stands now, given the choice, take the phakic procedure. Might decrease your chances of advanced AMD.

Written August 7th, 2017

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The Proper Magic Potion

Hi, home from physical therapy. My physical therapist and I looked all through the offerings of a world-famous corporation – gee, what could that be? – and picked out a new cart for me. See how this one works.

I came home from Penn State with my rotator cuff tendinitis flaring again. I had hauled my rolling crate around with some of the travel being uphill. Apparently not a plan. Not only do we become pack mules for all of the vision related stuff we get to haul around, we also get to have pack mule injuries!

How do other people handle the problems of – well, freight? Does anyone walk to the grocery? How do you haul everything? Any great ideas on carts?

I looked online for ergonomic carts and dollies and what they are showing is similar to what I just ordered. I will let you know if the new one is any better than the several I have purchased over the last year and a half.

FYI if you know someone who is mechanical and want to make some money, ask him (or her!) to design a rolling crate that can take punishment and not fall apart in three months! Not only would I buy one but I know several teachers and therapists who would also buy one.

That is the practical part of this page. Now for the not so practical but sort of cool part. Anybody ever read H.G. Wells The Island of Dr. Moreau? In that late 1800s science fiction novel Dr. Moreau creates human-animal hybrids using vivisection. Nasty business.

Today scientists are much more efficient than what Wells imagined. Today if scientists want a fish-mouse hybrid, they do it at a genetic level.

Madness, you say! (Cue demonic, mad-scientist laughter). Whoever would want them to produce a fish-mouse hybrid? Well, maybe you would.

Zebrafish are cool. They can regenerate parts. Put zebrafish genes in mice and they can regrow parts, too.

The parts the scientists are growing in mice are glial cells. The scientists have prompted the glial cells to become functional interneurons in mouse retinas.

Interneurons are connecting cells between other nerve cells. Remember I told you they are able to grow photoreceptors in eyes but cannot get them to connect? Interneurons are connectors. They receive and process signals from the rods and cones. With the proper magic potion for the job, scientists got adult mice to grow interneurons in damaged eyes. And the best part of all? They conducted signals!

This research was just published in July, 2017. It’s very early days and they have to work out many bugs, check for safety, etc. but it is the first step. Maybe some day they will inject photoreceptors into your eyes, inject zebrafish genes and magic potion, all over your lunch hour. By the end of the week you will have grown those new photoreceptors AND hooked them up to your optic nerve. Wow. Science fiction becomes science fact.

If you want to read the short version of the research findings, I found them in the ScienceDaily post. The date was July 26, 2017.

written August 1st, 2017

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Re-educating Our DNA

Back to the Genetic Home Reference. I have been seeing things that say gene therapy is one possible avenue of treatment for AMD and I have not been too sure what it is.

The Genetic Home Reference says gene therapy is the replacing of a mutated gene that causes disease with a ‘good’ copy of the gene. It may be used to deactivate a problematic gene or be introduced to help to fight a disease.

Because it is a new and potentially dangerous field of exploration, gene therapy is limited to diseases and conditions with no, known cures. That’s us, guys.

If you are not familiar with viruses, I offer a quick tutorial on how they work. Viruses are barebones ‘life’. There is debate as to whether or not they even meet criteria for being considered living organisms. Part of the definition of a living organism is that it can reproduce its own kind. Viruses cannot do that. Since viruses are no more than a strand of DANA wrapped in protein, a virus must ‘hijack’ a cell to make little viruses. The baby viruses eventually kill the host cell. This is why we get sick when we have a virus. Our cells have become factories/hosts for baby viruses. Sort of like the movie Alien in miniature. Yuck.

Since viruses have the ability to pierce cell membranes and mess with the cell’s ability to reproduce – effectively ordering the cell to reproduce a slew of baby viruses – it was decided they would be perfect for introducing ‘replacement parts’ into defective cell DNA.

The name for something that transfers things from one organism to another is called a vector. Therefore gene therapy uses viral vectors to get new DNA into cells. Researchers replace the basic, virus DNA with genetic material it hopes will repair the defective genes, then it ‘launches’ the viral vector to ‘attack’ and ‘hijack’ the cell.

How this relates to AMD is sort of basic. We know AMD is a genetically based condition. Change our genetics and we may eliminate the disease.

Johns Hopkins researchers have completed a phase 1 clinical trial during which they ‘infected’ retina cells with a virus carrying a gene that would cause the retina cells to produce a protein that interferes with the signals leading to the growth of new veins. The goal is to genetically alter enough cells they will produce enough of the protein to totally halt the neovascularization process and eliminate the need for shots.

Of course these studies are in very early days. One of the problems encountered was many people have developed resistance to the viruses use. They had met these enemies (the protein in the sheaths of the viruses) before and their defenses were in place. If the vectors are destroyed before they get to the targets, they cannot very well plant the new gene.

Still early days on gene therapy but it most definitely has promise. Remedial instruction to ‘re-educate’ our DNA may be on the way.

written July 16th, 2017

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Thank a Mouse

This page is just me being inquisitive. If you are not up for me trying to figure out biochemistry, you might want to skip this page.

Looking at the medications they are using for wet AMD and the new treatment for dry AMD, lampalizumab, I noticed something.  Most of the generic names end in -zumab. What the hey? What is that????

To begin with, I discovered there are two suffixes, -ximab and -zumab.  Wikipedia actually has a whole list of medical suffixes but I am concerned about two right now. Those are the ones related to drugs for AMD. Suffice it to know that every suffix means something.  -olol for example will always mean a beta blocker. Of the two I am interested in: – ximab always stands for a chimeric agent that responds to more than one antigen;  and -zumab always stands for a humanized antibody.

See what I mean about just skipping this page?

Chimeric.  Now I knew what a chimera is. A chimera is a single organism composed of cells that should have made up multiple organisms. The organism  is made of genetically different cells. According to MedicineNet human chimeras were discovered when it was noted some people have two different blood types. The generally accepted ways a human chimera is formed are for nonidentical twins to share blood in utero or for one to absorb the other.

Once again according to Wikipedia, chimera proteins are produced through the joining of two or more genes that originally coded for two different proteins. The properties of the new derive from each of its ‘parents’. Naturally occurring chimera are often found in cancer cells; thus, it would appear, the wisdom of using manufactured chimera proteins to battle cancer (a genetic version of fighting fire with fire). Chimeric cancer cells happen because of random genetic mutation. Chimeric proteins in drugs happen by design. Read genetic engineering.

Forging ahead here, every drug ending in -zumab is a ‘humanized protein’. And, no, that does not mean it is kinder and gentler. It means that the base protein used in the drug probably came from a mouse. Generations of lab mice have had the very stuff of their being manipulated in the search for ways to improve our health. Think kinder thoughts about the little devils.

Because – actually two becauses – there are a lot of similarities between mouse DNA and human DNA, we can use mouse as the frame for our designer drugs. Because some of their proteins are foreign to us and would cause an allergic reaction, the proteins have to be ‘humanized’. Potentially offending sequences are cut out and replaced by sequences found in humans.

The idea is to produce proteins that will get into a sequence of reactions and somehow change it. In dry AMD lampalizumab weakens the immune reaction. Wet AMD drugs intercept the SOS message being sent by the eye. That is the one saying the eye needs more ‘supplies’ and new ‘supply routes’ (blood vessels) should be built.

So that is the answer to that burning question (you really were dying to know; I know). If you are taking a drug ending in -ximab or -zumab,  you are the beneficiary of altered protein sequences. Be grateful. Thank a mouse.

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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 ways 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.

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Not Created Equal

We heard from a reader who has vitelliform macular dystrophy. I had never heard of it. Therefore you can image my surprise when I picked up an article I had downloaded last week and – guess what! – the article talked about vitelliform dystrophy! Sometimes the synchronicity in the Universe is scary.

Anyway, it appears the Universe has declared we are to learn about vitelliform dystrophy. Here we go!

I have discovered all macular diseases are not created equal. There are dozens of them and researchers are discovering more on a regular basis.

Vitelliform dystrophy may look like age-related macular degeneration and act like macular degeneration but it is not macular degeneration. (Don’t worry. We are not throwing you out of the group!)

Vitelliform dystrophy is a pattern dystrophy. They are so called because the damage tends to ‘draw’ things on the retina. For example, one manifestation of the disease looks like a butterfly (photo to the right is a fundus photograph of butterfly pattern).

Vitelliform 2 is called Best disease. This is not because it is the best disease to have nor is it because Dr. Best hijacked the disease and named it for himself. It is because the disease comes as a result of a mutation on the BEST1 gene. (Apparently that means we all have BEST genes and there are at least two of them. How about that.)

Best disease is a pattern dystrophy because – all together now! – it makes a PATTERN on your retina. The pattern is a sunny-side-up egg. The yolk is centered on the fovea.

One of the nice things about Best disease is you may never know you have it.  According to the Hereditary Ocular Disease site 7 to 9 percent of those with Best disease are asymptomatic. Others may experience vision loss but recover most of their function. A much smaller percentage may proceed to neovascularization and serious loss. Of course, the older we get the better chance we have of having some really serious problems. And by the way, children can have this one.

That is because, once again, it is genetic. Best disease is an autosomal dominant condition. That means it is on a body-forming chromosome – not the chromosome that has the x or the y and makes you a boy or a girl.  It is also dominant and can express itself whether or not its partner gene wants it to. You only need one of these babies to be in trouble.

Of course there are all sorts of things that may or will affect whether or not this gene does actually express. However, this is not a place to discuss epigenetics. Nor am I the one to explain THAT baby! Suffice it to say, you should warn everyone you are related to by blood that it has expressed in the family and they need to have regular eye exams.

Like AMD there is absolutely no treatment and no cure. (I get so tired of typing that). If you have Best disease and progress to CNV you may profit from shots.

And that, my dears, is that. Continue reading “Not Created Equal”

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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”

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