Category: Dry AMD

Slogging Through Again

I am waiting for my ride to go hot air ballooning and working on deciphering an article Lin sent me. Once again the question is how much loss can we expect from dry AMD, especially geographic atrophy? Regillo told me 60 degrees of arc loss would be extreme but my local retinologist said some people in their 90s can have GA encompassing the entire retina. Ouch.  [Lin/Linda: Sue wrote about ‘degrees of arc’ in her page Love Wikipedia.]

So, here be me again, slogging through another article I about half understand. Want to slog along? I would appreciate the company!

The article is entitled Clinical Endpoints for the Study of Geographic Atrophy Secondary to Age-Related Macular Degeneration published October, 2016. You there in the home audience feel free to download it and play along!

First of all, I latched on the statement (paraphrasing) “drusen may not result in actual visual acuity loss but the effects of having drusen can be seen in functional deficits very early in the disease process”. What functional deficits?

A 2008 paper by Feng Qiu and Susan Leat found people with very early AMD have loss of “low spatial frequency static contrast sensitivity”. Yippee. Once more down the rabbit hole. It appears – according to the appendix of Emergent Techniques for Assessment of Visual Performance – spatial contrast sensitivity has to do with lighting, the place on the retina where the image is falling and something called field size as well as time factors and the orientation of the image.

Boiled down it has something to do with how sensitive we are to variations in the data our eyes are gathering. I think. Don’t hold me to it. Just know that 20/20 vision with drusen might not be as perfect as we might think.

We talked about reduced dark adaptation before and this is also a problem in early AMD. Apparently there are several effects early drusen have that have nothing to do with acuity.

The next thing I had to look up – in the same paragraph, mind you! – was information that might help me understand a statement suggesting advancement to GA from early AMD may in part depend upon the presence of “reticular pseudodrusen”. So now we have drusen impersonators????

According to Association of Pseudodrusen and Early Onset Drusen by De Bats, Wolff et al (doesn’t that team sound perfect for the Halloween season?) pseudodrusen form on top of the RPEs and not below them as do ‘real’ drusen. There seems to be a connection between having ‘eye poop’ aka drusen on top of the RPEs and early and rapid develop of advanced AMD.

And the above was all in one paragraph! I may be a very long time in deciphering this baby.

So what I have discovered so far is this: visual acuity does not tell the whole story about functional vision loss when it comes to early AMD. If you have drusen be aware your contrast sensitivity and dark adaptation are probably already compromised. Secondly, pseudodrusen, which is eye poop on top of the RPEs, can predict a more rapid and earlier progression to GA.

Have I found a thing about GA outside of the macula? Not yet, but I am still reading! Talk at ya later!

written October 7th, 2o17 Continue reading “Slogging Through Again”

Rookie in Training: Part 2

My family doc referred me to an Ophthalmologist in 2008, after a Walmart Optometrist told me I had cataracts. I’ve been going to this eye doc annually and he told me to take AREDS2 and use over the counter lubricating eye drops. He started mentioning that I had drusen and this August, I asked him point blank – “Do I have AMD?” I don’t know if he would have given me an official diagnosis if I hadn’t forced the issue. He saw blood in my left eye, so did Fluorescein Angiography and referred me to a Retina Specialist. I had doubled up on my Aleve (naproxen) because of pain from a dental procedure and told him that was probably the cause. He thought I had developed high blood pressure or diabetes, or possibly Wet AMD.

Two weeks later, I had my first appointment with the Retina Specialist. By then, I had cut back on the Aleve and the blood had almost disappeared. He did an OCT of my macula for both eyes and said I had dry AMD but was fine otherwise. No wet AMD. I also went back to my family doc who agreed with me that it was probably the Aleve.

Neither of my eye docs ‘believes’ that my DNA could affect the how eye vitamins work or don’t work. The retina specialist thinks future research will debunk the research that showed zinc being harmful to some of us. If AREDS2 is the only recommended eye vitamin, they refuse to consider alternatives. And they refuse to prescribe the ArticDX genetic testing. Although I am a rookie with AMD, I feel like I am more educated on AMD than either of my specialists, thanks to Lin and Sue and all of you.

Until I can figure out my DNA, I am taking the Walmart Vision Formula 50+ which has only 9 mg of zinc. I was already taking extra zinc every time I caught a cold – or thought I might catch a cold – and I have cut back on that and take an extra 25mg with the meal when I am not taking the eye vitamins. (That magic potion to strengthen my immune system also includes 500MG of Ester C and Echinacea.)

I’ve been using an Amsler Grid for a few years now and try to eat healthy. I never smoked. So for now, I think I am doing all that I can. I feel like I am ‘in training’ for a future with AMD. I will follow the research, donate to the foundations supporting research, and let Lin and Sue be my coaches. Knowledge is power.

Back to Our Guest Authors: Their Stories

Rookie in Training: Part 1

by Joann Davis

Because my mother and grandmother both had AMD and my son found out he had AMD genes when he did 23andMe DNA testing several years ago, I have been waiting for my diagnosis for years. I was involved in a Jules Stein Eye Institute GARM II study for people under the age of 65 with parents with AMD but no diagnosis yet. I was so pleased to find Sue’s blog and the Facebook Group and was an early ‘joiner’. I hated the play “Waiting for Godot” and hated “Waiting for AMD”. [Lin/Linda: just checked & Joann has been a follower of our website/blog for 1 year and 5 months…wow, she was one of the first!]

I wish I had taken a more active role in my mother’s eye health. She had cataracts removed at an early age (56) and always ate healthy because she knew that was the best way to stave off AMD. I remember the ‘Swiss Chard’ year when she was eating a lot of Swiss Chard. My dad had a big garden, so she had access to lots of fruits and vegetables. She always said “My mother got AMD when she was in her 80’s and I didn’t get it until I was in my 90’s”. (Makes me feel like a failure to be diagnosed at 70.) I bet she really had dry AMD earlier than her diagnosis. She also had Glaucoma. She had one or two shots in her ‘good’ wet eye, and thought it made it worse, so didn’t get any more shots.

Because of her age, she was having other health problems which made adaptive technology a challenge. Again, I wish I had been more proactive. She was using hearing aids and having small strokes, had serious gall bladder and colon issues, high blood pressure, and arthritis. Because she used a walker, she didn’t get the exercise she was used to. She was on a restrictive diet so she couldn’t eat the healthy fruits and vegetables anymore. She never completely lost her sight, but I know she was depressed as her world kept shrinking. She lived to 95 1/2, and passed away in 2012.

Next: Rookie in Training: Part 2

 

About Joann

Joann Davis is 70 and has recently been diagnosed with mild dry AMD in both eyes. Her mother and grandmother both had AMD and her son has the genes. Joann also has cataracts, floaters and dry eyes. With glasses, her vision is 20/40. Joann spends most of the year in northern Illinois and the winters in Ft. Myers, Florida. Joann is retired but very busy with numerous board memberships. Joann exercises every day, beginning with yoga, crunches, planks, ‘boy’s pushups’, weights, and then a long walk. Joann wants to do as much travelling as she can while she can still see and is heading to Italy soon and plans to go to South Africa next year. Joann’s career was in technology and cyber security sales, and she still belongs to cyber security organizations where she gets to hang out with the FBI and Secret Service.

 

 

My Friend in Manila?

Happy Tuesday! Waiting for the van to go to school. Yesterday I was picked up at 6:56 to ride 9 miles and be there by 8:30. Dare I say I was not pleased? I just keep turning my mind towards acceptance (DBT alert!).

This is the way it is in my life now and I need to accept such nonsense if I am going to get where I need to go.

Today is day 61 of “your dog is dying.” We took a nearly 40 minute walk yesterday. Pretty active ‘dead’ dog. One day at a time.

I continue to monitor for information on lampalizumab. As of yesterday, September 11, all the news was still financial, but not quite as doom and gloom-ish for Hoffman-La Roche. Just sit tight on that one.

Apellis is drumming up excitement for their geographic atrophy treatment, APL-2. We talked about this before. APL-2 decreased the rate of atrophy growth 29% as compared to sham when injected monthly and 20% when injected every other month. In the second 6 months of the trial the reduction was 47% in the monthly injection group. APL-2 now appears to be the ‘show’ to watch as they go into phase 3 clinicals.

Philip Rosenfeld wrote a short blurb for healio.com. His disclosure statement said he has investments in Apellis. Either he is talking up the product, is truly sincere, or putting his money where his mouth is. In any case, Rosenfeld remarked APL-2 worked across a genetically diverse population sample. There were no stars and no non-responders.

Unfortunately, Rosenfeld also remarked that there is more of a chance of dry AMD developing into wet AMD when APL-2 is used. His opinion was it would have happened anyway in the eyes that became wet, but that will require more research.

We will keep an eye on APL-2.

10 hours later: The van came at 8:01 and had two people going to the local hospital already on it. Late for work? You could say that. Once more the shortcomings of transportation here are giving me fits.

Next, this has nothing to do with eyes but it happened to me today and I do want to mention it. I got an email from a ‘friend’ asking for a ‘favor’. Since my friend lives in Florida I was thinking it was hurricane related.

Turns out it was a scammer ‘phishing’ for money. My ‘friend’ was stuck in Manila and needed $2000. Yeah, right. I asked a couple of questions, obscure stuff that only members of the group I hung with in my 20s and 30s would know, and that was the end of the communication. Maybe my real friend was not stuck in Manila at all!

It appears many people in the world think of Americans as rich and gullible. I am definitely not the first and I try hard not to be the second. I assume it is the same for you.

If your ‘grandson’ emails or calls for ‘bail money’ from Tijuana, be sure to ask a few, HARD, identifying questions. Something that never got online. If the ‘IRS’ or the phone company or gas company or whatever calls and gives you a phone number to call with your credit card number, have someone look up the number independently and call that number to inquire.

Just another public service announcement.

Will check in again later!

written September 11th, 2017 Continue reading “My Friend in Manila?”

Bad Patches

Today, September 8, 2017 started and sort of ended with mini pity parties for me. We had a speaker this morning and I needed to go to the office ‘annex’. For some reason transportation decided they needed to get me to my 8:45 meeting at 7:30. Never going to understand that.

I was accepting of it and took along things to do for an hour. I am getting used to the indignities of the state subsidized transportation system.

After all, I am ‘handicapped’ and ‘elderly’. (You know I find that hysterical; don’t you?)

I was okay with it until my colleagues started to cluck their tongues and make a fuss over the absurdity of it all. Apologies for not thinking to offer well ahead of time and promises to do better. I was chastised for not asking by half the room. Then I had to fight the impulse to cry.

Not sure what upset me. It could have been being reminded it is not fair, whatever that means. It could have been their willingness to help. It could have been being reminded I am now different. Maybe a combination.

Whatever it was, sometimes it just smacks me (you, too?) between the eyes. Believe it or not, I am often able to forget I am now handicapped/disabled/impaired/whatever. Other times….I am sitting by myself an hour and a half early and people feel sorry for me and I feel sorry for myself and that is all she wrote.

The rest of the work day went great. Busy and sort of productive. Of course, I had to get a ‘seeing eye colleague’ to read a particularly blurry fax to me, but that was not a problem. People help.

(Of course this was the same colleague who was making the cracks about allowing the one, ‘blind’ staff member to cut the baby shower cake we had for another colleague! News flash: I could not cut equal pieces when I could see! Bringing to mind a corruption of an old joke: “Doctor, if you fix my vision, will I be able to cut a straight line?….Funny, I couldn’t do it before!” Da dum dum!)

And fixing eyes brings me to the second letdown of the day. I – and I believe others – have been thinking lampalizumab was a slam dunk. It was going to go breezing through the phase 3 trials and help to cure the world. Did not happen. Lampalizumab failed to show a statistically significant effect as compared to sham and the one trial has been terminated.

I looked all over the web trying for specific information and all I found was the press release repeated by about eight, different services. Not sure what happened and I don’t believe they know what happened. Here’s one version of the press release from BusinessWire.com.

Not that I am anyone you should listen to, but I would recommend not giving up yet. They still need to further analyze the data. It is possible they got a split just as they did the last time. Maybe 75% of the samples were non responders but the other 25% responded with a 40% slowing of the degeneration. 0 + 0 + 0 + 40 divided by 4 is 10. An average of 10% would not meet criteria but the 40% would.

Just wait and see. Some days have bad patches, yes, but they often are just that, patches. In the big picture, we are doing okay. Keep on keepin’ on.

written September 8th, 2017

Continue reading “Bad Patches”

Research: Dry & Wet AMD

Hello! I am going to get to the article Lin found on BrightFocus Foundation’s website about ‘lamp stuff’ aka lampalizumab but first I wanted to quickly mention a Google Talk by Isaac Lidsky. The title is Eyes Wide Open.

Lidsky began losing his sight to retinitis pigmentosa when he was 13 years of age. Although he has been totally blind for many years, Isaac Lidsky is extremely accomplished and has developed a philosophy that includes all sorts of concepts such as being present in the moment, doing what works and not abdicating responsibility for your life to your personal heroes and villains. His half an hour Google Talk may make some people rethink their attitudes towards their sight losses.

While I don’t expect many people to feel ‘lucky’ they are going blind – and Lidsky does consider his blindness to have been a blessing – Lidsky’s perspective on things can be thought provoking.

OK, onward to ‘lamp stuff’. We have quoted Joshua Dunaief before. One of the most helpful things he does for me in the current article is give us a pronunciation guide for lampalizumab. It is lamp-uh-liz-you-mab. Sort of like “Lamp!…uh, Liz, you mad/b?” You know, what you say when you knock over Elizabeth’s favorite light.

We have gone over the study results already in these pages. Complement factor I variant folks got kickin’ results. The rest of us, not so much. A reason for genetic testing for us before we submit to needles in the eyes, literally!

Dunaief says results are expected in 2018. Yep, December is their target date for publication. He does not mention phase 3 is over this December as is indicated in clinicaltrials.gov.

So, basically, still not really sure what is happening with ‘lamp stuff’ and me. May be offered it in December. May not be. May accept the offer. May not. I would love to know my genotype as compared to the SNPs they found in the experimental sample. Being a responder would be incredible. Being a nonresponder would be very bad. Dilemma.

And information for our ‘wet’ friends for my last 200 words. In JAMA Ophthalmology Jackson, Boyer and Brown reported the results of an experiment with an ORALLY administered vascular endothelial growth factor (VEGF) inhibitor. In other words, they have been experimenting with a pill they hope would do the same thing as your anti-VEGF shots.

The stuff is a tyrosine kinase inhibitor. It caused a lot of upset tummies and diarrhea (5 and 6 subjects out of 35 respectively) but the side effects were not bad enough to stop the experiment. Some people did stop because of liver problems. Those with liver issues would probably not be candidates for the treatment.

Only 40% of the total required rescue shots. Even those people received fewer injections than they had without the pills.

Before you all rush out for your X-82 pills, bear in mind this was a phase 1 experiment. That is safety and tolerability, guys. They are moving on to proof of concept, phase 2, with a bigger n. (n being the number of subjects in the study, remember). Check clinicaltrials.gov if you are interested.

Remember we all do our part in this fight. If you have a strong liver and a strong stomach, X-82 might be your kind of research. You might get to be a lab rat before I do!

written September 2nd, 2017

Continue reading “Research: Dry & Wet AMD”

Timeline Part 1: Advances in Treatment & Care for People with Macular Degeneration

It’s Lin/Linda.  I created this page to go with Sue’s page Not Your Parents’ AMD.  Like some of you, I had a loved one with AMD.  It was my father who was diagnosed with AMD in 2005 at the age of 82.  At the time, I was living 700 miles away and I did not know much about the disease or at what stage he was diagnosed.  He progressed to geographic atrophy (GA), that much I knew.  He was the sole caregiver for my mother who had Alzheimer’s Disease.  He continued to drive (not safely), take care of her and the house.  He was never referred to vision rehabilitation or offered any help other than being told to use handheld magnifiers.

I wondered how things have changed since then which led me to do this timeline review.  Not only have there been advances in the medical end of the field but also in the technology that is allowing people to remain independent for as long as possible.  That is if a person learns how to use the various devices and apps available.

I’ve based the categories of time on an article Age-Related Macular Degeneration
1969 –2004: A 35-Year Personal Perspective by Stuart L. Fine, MD published in 2005.  He says “In 1969, patients with AMD constituted a small part of a typical ophthalmic practice. From 1969 to 2004, the prevalence of AMD has increased, and the methods of evaluation and treatment have changed dramatically.”

I know I have missed many events that have been critical to the history of the treatment & care of AMD.  There is SO much information out there and I’ve tried to use the most significant dates I could find.  Have a suggestion of what to include? Did I get a date wrong? Let me know in a comment or send me an email at light2sight5153@gmail.com.

1st Era: 1969–1979
  • Emergence of fluorescein fundus photography: test used in diagnosis of retinal diseases
  • Development of ‘hot’ (high power) laser photocoagulation, first treatment for wet AMD
  • Relationship of drusen to age-related macular degeneration
  • Other developments:
    • 1976-1977 first personal computers affordable for home use
    • more low vision aids:
      • 1960s large print books became available
      • 1976 large print calculators became available
      • 1969-1970 CCTV (closed caption TV) for reading aid
2nd Era: 1980–1994
  • Clinical trials to evaluate new treatments, especially laser photocoagulation (1979-1994)
  • Development of risk factor data from large and small epidemiologic studies (epidemology is looking for patterns & causes)
  • mid-1980s term ‘senile macular degeneration’ becomes ‘age-related macular degeneration’
  • Other developments:
    • 1982 Vitreous Society was founded; 1983 first meeting attended by 44 retinal specialists
    • 1991 OCT (Optical Coherence Tomography) test used in diagnosis of retinal diseases
    • mid 1980s name changed from ‘senile macular degeneration’ to ‘age-related macular degeneration’
    • 1992 Americans with Disabilities Act (ADA)
    • 1983 first cell phones
    • 1991 World Wide Web for ‘surfing’ the Internet with easy-to-use browsers
    • low vision aids:
      • MaxiAids catalog of aids for orders from people with low vision & other impairments
    • technology/low vision aids:
      • 1982 DragonSystems founded Dragon NaturallySpeaking, speech to text
      • 1988 ZoomText was released which is software to magnify text on a computer screen
3rd Era: 1995–2003
  • Evaluation of radiation therapy for neovascular AMD, not proven to be effective
  • Assessment of pharmacologic interventions for neovascular AMD; Photodynamic Therapy (PDT) “cold” (low power laser) with Visudyne (first drug treatment;  2001)
  • Prevention trials: results AREDS released 2001
  • Other developments:
    • 1995 Amazon sells books online (1998 expands beyond just books; e-books 2000)
    • 1996 Google released
    • 1998 first e-book reader The Rocket
    • 2000 GPS available for civilians; 2001 personal navigation systems available like Garmin and TomTom
    • 2000 Microsoft & Amazon sell e-books
4th Era: 2004 – 2017
  • Completion of ongoing trials for neovascular AMD: FDA approval: Macugen 2004; Avastin 2004; Lucentis 2006; Eylea 2011
  • Earlier identification of eyes at risk: regular use of OCT (Optical Coherence Tomography) and other diagnostic tests
  • Prevention trials: results AREDS2 released 2013
  • Increased number of retinal specialists: eg, American Association of Retinal Specialists (ASRS), formerly Vitreous Society (see 1982 above), has 2700 members representing 60 countries.
  • Other developments:
    • 2011 First baby boomers turn 65
    • 2004 Facebook
    • 2013 first ‘bionic eye’ retinal implant, Argus II approved by FDA
    • technology:
      • 2007 Amazon Kindle e-reader; iPhone & Apple IOS
      • 2008 Android 1.0 & Android phone
      • 2010 Apple iPad
    • technology/low vision aids:
      • 2005 Apple VoiceOver for Mac users
      • 2009 VoiceOver added to iPhone IOS
      • 2010 FDA approved implantable telescope
      • smart glasses/wearable technology
      • 2014 KNFB Reader app for Apple & Android; 2017 for Windows 10
    • ongoing research areas:

I Want to Be a Mutant

I want to be a mutant. Oh, not like the X-Men although it might be cool to be Storm. I want to be a mutant because those are the people who respond the best to lampalizumab.

A friend emailed me an Associated Press piece entitled Drug shows progress against vision-robbing disease in seniors. Although this was the first time I have heard this, according to the article, ‘lamp stuff’ doesn’t do a bit better in people with the specific gene mutation, it does a LOT better!

I had heard that lampalizumab produced a 20% regression in lesion progression. That, folks, appears to be an average.

Those with the complement factor I risk allele actually had a 44% reduction in geographic atrophy progression. Wow!

To me, this is the first BIG indication genetic testing and AMD treatment have to be closely associated. I really do NOT want to be poked in the eye with a needle every month if the treatment won’t do any good. Likewise, I will be more amenable to said needle poking if I know I have the gene and I can slow my vision loss by nearly half. Not to mention how insurance companies would respond if they knew they could save money by eliminating non-responders from the pool.

Now, you need to remember all of the hard sciences are not my forte, but it seems to me complement factor I is a molecule that helps to trigger the action of the immune system. Remember all that stuff about whether or not AMD is an autoimmune disorder? It appears complement factor I is able to slow down some aspects of immunity that are running amok and attacking the good guys as well as the bad. Once again the theory appears to be our sight is being wiped out by friendly fire.

Musing here a moment, I have a very strong immune system. Never had mumps or chickenpox. Only had one form of the measles. In the 50s and 60s when I was small, kids got those things all of the time. Once more, I was the odd one. But what if my great immunity is not the result of a strength but actually of a weakness? To wit, I have an immune system with bad brakes. That is a thought. After vanquishing all the bad germs, it turned on itself. Put that with a strong family history of RA, another autoimmune disorder and it makes you wonder. Things that make you say Hmmmm….

Anyway, lampalizumab tightens loose brakes on immune reaction in those who have the complement factor I risk allele. It keeps the immune system from running wild and reduces the rate of damage about 44% in geographic atrophy.

I don’t believe the genetic testing we were given for trial measured the complement factor I risk allele. However, I should suspect changing the genes they highlight may not be that big a job. I also suspect making that adjustment would be a big moneymaker (This is America, after all).

So, next we should probably all find out if we are mutants. I have dibs on being Storm. Who wants to be Wolverine or Charles Xavier? [Can I be Wolverine? Love what he does with his nails!]

written June 28th, 2017

Continue reading “I Want to Be a Mutant”

Geez, It’s Dark in Here!

Back again. I don’t want to scrub the floor or score a test, soooo….a page!?

Still checking out short blurbs from Modern Retina. Rosenfeld reported that low-luminance visual acuity deficits are predictive of the rate of geographic atrophy (GA) progression. Low-luminance visual acuity is basically night vision.

Following up on this I discovered that back in 2008 Janet Sunness found GA patients who reported poor night vision were much more likely to go legally blind than their GA peers who could see better at night. These people made up the quarter of their GA patients (visual acuity of 20/50 or better) who became legally blind within four years.

I believe them but still have a couple of questions. Recovery time from being ‘blinded’ by bright light is forever for me. Leave me there and come back in an hour.

Night vision is not bad. I prefer to walk without a flashlight because I see better to navigate. How can that be considering I am one of those who became legally blind?

The study measured night vision by seeing how much could be read in low light conditions. Reading in low light, I am not so good. Maybe that is the difference.

Anyway, if you cannot afford a lot of fancy testing, seeing how much you can read at dusk may give you some idea of how bad things are going to get. Just what we want to know; right? How bad things can really be.

And in other news, inflammation remains a target for the AMD researchers. Lampalizumab, aka ‘lamp stuff’, blocks complementary factor D to help control the alternative complement pathway (that thing again!) and reduce retinal inflammation. ‘Lamp stuff’ is said to work with carriers of the complement factor I at risk allele. Considering​ Regillo wants to start poking needles in my eyes come 2018, I cannot help but wonder if I actually have that gene. I would hate to be poked in the eye every month to no good end.

Maybe I would rather use POT. ?That’s POT 4. POT4, aka APL 2, blocks all three pathways of complement action at the same time. They are looking to develop an intravitreous shot that would be very long-term. None of this four to six weeks business.

And talking about shots, I just lost the article somewhere in this mess (not domestic goddess material; remember?) but I also read a short article taking about a new, medication delivery system they are working on in the UK. This team has been working on developing a little, bitty molecule that can permeate the layers of the eye and deliver medication to the retina through daily eye drops and not monthly shots. Not only will the people getting the shots approve, but the NHS (National Health Service) will approve because it will cut the number of office visits way down. Save money. Ka ching! [Lin/Linda: never fear, I found the article, click here.]

So there you have a review of some of the articles I pulled off of Modern Retina. They have lots in the works. Some of it is promising and some proves not to be, but they are zeroing in on treatments (plural because with a condition caused by multiple genes I believe there will be multiple avenues of attack). We are getting closer to answers. There is hope. Continue reading “Geez, It’s Dark in Here!”

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!”

Not Your Parents’ AMD

3 pm Monday and so far it is a good day. The pool guy is working on my new liner. The funny thingee on my tummy is a normal, benign growth and the transportation company got new vans with fancy logos painted on them. No more confusion with two dozen, white vans. Life is looking up!

Lin told me there was a conversation thread in the Facebook group about parents who struggled with AMD. People remember what their mothers and fathers went through and they are determined not to become like them.

I am reasonably sure my father’s vision problems were AMD. The more I think about it his father’s vision problems may have been AMD. I remember both of them using a handheld lens to read the newspaper as well as the really strange interpretations Daddy would have when it came to TV shows. I have no idea what HE was watching but it was not the same thing I was watching!

I have said it a couple of dozen times and I will say it again: this is the best time in the history of the human race to be losing our sight. Absolutely the best. You may not realize it. You may remember what you saw and think we are doomed to go there too but we are not. We really are not.

I tried a handheld magnifier for a couple of weeks. Not doing that again. They are very inefficient. I have my CCTV, my handheld reader and my iPad which can go in the Justand.

[Lin:Linda: To see what Sue uses on a daily basis, check out these pages: A Day in the Life and A Day in the Life:Work Day.]

I can get newspapers on my phone and books from BARD (there are other sources, too, as well as magazines which are available).  I’m able to take a picture of pretty much any text I want and my KNFB Reader will read it to me. The zoom feature on my iPad will allow me to read email and research pretty efficiently. ZoomText allows me to work. (refer to the “Day in the Life” pages above)

If I want to look at something a little distance away I can use my max TV glasses or my monocular. Not too bad.

Depending upon when Lin publishes this page, you either have or will be hearing about audio description services (coming soon!). If my father had had those for the TV we would have been “on the same page” a lot more than we were when we watched programs together. Audio description can also allow you to go to the movies and live theater and actually know what is going on.

Do I want to be losing my sight? Hell, no! This is not a walk in the park but it is not what Daddy endured either. Just the same he made it into his mid 80s and managed to take care of himself until other issues brought him down. If he could do it without all of the toys, I can do it.  [Lin/Linda: My dad had geographic atrophy & took care of my mother who had Alzheimer’s using several different handheld magnifiers & a few other low vision aids.]

Yet another reason to be optimistic is all of the exciting research happening. We are poised for a veritable explosion of treatments. Not cures, mind you, but treatments. Thirty years ago there was nothing.

[Lin/Linda: To see what’s in the research pipeline, click here.]

What can you do? Be willing. Use what has been provided. If you put that iPad your son gave you in the drawer you have absolutely no grounds for complains. Bluntly put? Your extra suffering will be your own damn fault.

What else? Volunteer. Sign up for clinical trials. Join support groups. Share your knowledge and skills.

Life – and this vision loss bit included – is the craziest thing you will ever experience and none of us get out alive. Make the most of it while you can.

Continue reading “Not Your Parents’ AMD”

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”

Hodge Podge

This may end up as another chatty, hodge podge affair. There is really nothing major happening and in the world of progressive eye disease nothing major happening is a good thing!

So, actually, I guess that is my first offering here. Those of you who have recently received your diagnosis or have had a crisis and are really distressed – it is not all drama and disease focus for the rest of your life.

You adjust and other things take center stage. That is not only normal but it is a good thing.

Second offering is something I picked up last month at the support group. When I said dry AMD is the base disease, they looked at me as if I had three heads. What I meant – and what they had not gleaned. Why won’t people do their research! Or minimally ask questions? – is that even though the shots have stopped the neovascularization, the growth of new blood vessel that lead to a bleed, you still have the underlying cause of the problem. The cause is regular, old, dry AMD.

This is why, even though you think the stuff we publish on dry AMD does not relate to you, it does.

Wet AMD is one type of end stage AMD and geographic atrophy is the other. Stopping the bleeding does not eliminate the underlying disease. It just eliminates the symptom.

Which brought me to another thought. I have never seen anything that says if an eye prevented from going wet will go to geographic atrophy. Hmmmmm…..

Nuts! More to worry about. Kaszubski et al in Geographic Atrophy and Choroidal Neovascularization in the Same Eye: A Review stated there are people who can have both forms at the same time. Geographic Atrophy generally happens first. (That part is bad news for me although I am under the impression that for me there is very little left to ‘save’ by building new blood vessels.)

To follow the question posed above, though, they also say there is some evidence anti-VEGF shots can increase the chances of GA development.

While that is bad news for you getting the shots it does NOT mean to stop your shots. No shot and you will bleed. Bleeds lead to scarring and certain vision loss now. GA is slow and lead to vision loss later. Given a choice, battle the bleeds and worry about the atrophy later.

End of lecture.

Other than that, in real time Memorial Day approaches and I am thinking summer. Although I know there is ‘no rushing city hall’ (to paraphrase another old chestnut), I started looking up Astellas and Robert Lanza again. Just to see what the dear boy is up to. I have been hoping to get to Philly and the clinical trials this summer. It would be perfect timing for me but I am not sure about the Astellas Institute of Regenerative Medicine (AIRM). They will need to give Wills the go ahead to start one of ‘my’ clinical trials before anything happens for me.

Astellas is gearing up for something, though. Something big. A couple of years back they bought OCATA for $379 million. Now they are on a hiring binge and are looking for a bigger location in or near Marlborough, Mass.

In the business articles I read Lanza purposely hyped the work they are doing on AMD. I am assuming that is still their big thrust. (That is even though AIRM is in a variety of areas of regenerative medicine and Lanza himself is intellectually all over the place, including developing a theory of the Universe!)

Anyway, seeing this big a build-up with lots of business chatter tells me something is going to happen. Just hope it is in the trial I have volunteered for. My eyes and I are not getting any younger! Continue reading “Hodge Podge”

Hindsight is 20/20

Good evening! How are you all?

Lin has noticed I seem to have written soooo many pages they are overwhelming and confusing some people. She feels this is particularly true for some of the newbies who probably feel like they have walked in on the (boring and confusing) middle of a movie. [Lin/Linda: to be clear, those are Sue’s words! ::grin::]

Understood. Some of you are back in the shock and doom phrase and I am talking about getting newspapers on your phones and other trivial matters. Who wants to hear about that sort of thing while your world is unraveling?

In the interest of pointing you towards something that might actually be helpful, Lin is republishing some earlier pages for your attention and discussion. And I – always helpful – am going to add to the confusion by writing another page!?

This page will have a catchy title thanks to Lin, but right now I am going to call it “What I know now that I wish I had known a year and a half ago”.

First, you are not going everything black and dark blind.

It is not good but neither is it quite that bad. You are losing central vision. Things will not be good for anywhere from about 15 to 60 degrees of arc. Since normal visual fields are 170 or so degrees of arc, you have the potential to lose about a third of your vision. Not anything to cheer about but better than 100%.

You may not be doomed to progress to end stage AMD.

About 15% of patients become ‘wet’. About 15% progress to geographic atrophy. That means you – starting out with drusen and a diagnosis of early AMD – have a 85% chance of dodging the proverbial bullet for end stage AMD. You may very well not get as bad as I am and a year and a half after my second eye went to hell, I am still functional. [Lin/Linda: a person can have both wet AMD and geographic atrophy in the same eye.  I don’t what that does to the %, if anything.]

You did not cause this.

Yes, AMD is caused but it was not caused by anything you did or did not do. The causes are in your genes. This is a heritable disease. There are dozens if not hundreds of genes that are being investigated to try to figure out how AMD is created. It appears AMD may just be the result of a genetic ‘perfect storm’ and there is no one to blame.

There may come a time you are seeing things.

I saw some odd stuff when my brain was working overtime to assign meaning to the faulty images my eyes were sending it. You are not psychotic (I hope you are not psychotic). This is Charles Bonnet Syndrome. When your brain gives up trying to assign meaning to false signals you will stop seeing weird ‘stuff’. In the meantime, enjoy the fantasy.

Point number last: There is an amazing amount of hope for treatment and eventually a cure for AMD.

Research is going on everyday. New discoveries are announced with regularity. The medical community is hot on the trail of something that will arrest the progression and may even reverse this disease. All we have to do is hold on.

OK. Those were my biggie when I first lost my second eye. What are you worried about? Please share and we can discuss it. Continue reading “Hindsight is 20/20”

Shimmering

Albert Einstein once said “the more I learn, the more I realize what I don’t know.” Apparently I am in good company, because I feel the same way.

With no immediate crises in my life and no immediate reason to freak out – and even with geographic atrophy and permanent retina damage, this state of affairs is possible! – I have been trying to get caught up with some research. I keep running into things I have no knowledge or understanding of.

Lin suggested that after over a year we should know SOMETHING about these things. We don’t. For example, I am still clueless about what I can expect concerning the progression of density of my ‘blind spots’.

And speaking of disease progression, (was that a smooth segue or was that a smooth segue??), I do have a couple of things to say about disease progression from that last article I read. Remember the one on GA?

The article opined all the new interest and hoopla about dry AMD came from the success with treating wet. However it wasn’t why I would think. You know, we have scaled that mountain and are looking for new summits sort of thing? Nope, the reason was they discovered that even after severely limiting the development of neovascularization in eyes, the eyes just kept right on progressing with dry AMD! Sorry, darlings.? It seems a former wet AMD eye becomes a dry AMD eye.

And dry AMD – to my great chagrin – progresses. How much? I assume it can take the entire macula but I have not seen that definitely stated anywhere. I have seen it stated that it generally stops with the macula. Maybe not such a ‘small’ favor. Could be a lot worse.

The last thing I learned from that article is how best to document disease progression. That is with something called cSLO FAF. Isn’t that informative? Exciting even!

OK, OK, just ‘funning’ with you. I looked it up. Fundus autofluorescence is diagnostic imagery. It detects fluorophores in the retina. Fluorophores being chemicals that re-emit lights shone at them. Research quoted by Wu in Use of Fundus Autofluorescence in AMD said risk of wet AMD can be predicted by a patchy reflection pattern and lots of ‘shimmer’ (my word) at the edge of a patch of geographic atrophy is predictive of cell death and growth of the GA. The more ‘shimmer’ the worse the trouble you are in. [Lin/Linda: We hadn’t had a music reference for some time.  When I hear the word ‘shimmer’, I think of John Lennon’s song “Julia” which uses the word ‘shimmering’, hence this page’s title. ::smile::]

So if anyone throws a bunch of letters ending with FAF at you and says you are going to have that, it may be they are checking for disease progression. I cannot remember ever having one, but it is noninvasive so no biggie. Should not hurt. Just more pretty pictures. Hopefully they will find something good.

Pretty much it for now. Will probably write some more nonsense between now and then, but Wednesday I am going to another support group meeting. They are demonstrating an electronic monocular called a Mojo and I want to see it. Will let you know!

Chat with you later!

 

written May 6th, 2o17 Continue reading “Shimmering”

Islands of Damage

I have got about 45 minutes before I need to get ready to walk and go to yoga. Had to go to my third job today, just for the half day. My husband took me up and did errands for the morning, then we went to lunch and picked up my framed photos for the contest in the fall. I am four months ahead of the game but I had to pay extra to get them done on time once before. Not doing that again.

Lin gave me an article entitled “The Journey of ‘Geographic Atrophy’ through Past, Present and Future”. Started reading it …finally… today. First thing I read is GA is ‘end stage’ dry AMD.

I knew it was advanced AMD but never gave a lot of thought to it being end stage. Does ‘end stage’ just mean the last stage or does it mean I have almost reached the end of the deterioration? Need to read on.

There is depigmentation of the cells This is a problem because it is the building up and depletion of pigment that allows us to see. In GA you can get to look in and see choroid blood vessels with no difficulty, as well.

I have seen images of my blood vessels in my choroid. Nothing between them and the camera. Essential, my choroid posed naked.?

The article said seeing the degree of degeneration even with the new technology is difficult. That is apparently why my retinologist saw no change in my scans even though I was perceiving an increase in density of my left scotoma.

The article also said there is high variability in the location, number and shape of individual lesions. The makes sense considering my blurry spot is up and right when looking at the Amsler Grid and my ‘sweet spot’ for eccentric viewing is lower and a little to the left. In other words if I center my poor, wrecked fovea at 1 or 2 on the clock face, I can see things between 9 and 3, courtesy of my ‘sweet spot’. Other people are different, of course. Putting each fovea on the center of the Amsler grid and seeing what blurs out can help you chart your scotomata. Then, learn to work around them.

I am not sure if this is good or bad. Exception in a limited number of cases, the fovea is spared until the end. Does that mean I am actually more abnormal than I have always believed or does it mean I am at the end of the process? Dunno.

See why I feel like a mushroom???? Jeez. Need information here!

Geographic? It appears early researchers (and by ‘early’ I am referring to the 1970s! Research and discoveries are traveling at light speed and there is no reason to lose hope something else helpful will be discovered soon) thought the sharp demarcation of lesions like ours looked liked borders of islands and continents as drawn on a map. That is where geographical came from. We have islands of damage in seas of healthy tissue.

Ok. Gotta run. There is lots more in the article though. Will let you know. Continue reading “Islands of Damage”

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”

Biochemistry Redux

Doxycycline and I have a ‘history’. Not totally a good one. Doxy is the medication given prophylactically when you are bit by a tick. Some doctors recognize waiting for the red ‘bull’s eye’ of Lyme disease before treatment may not be a good idea; others don’t.

The second time I was tick bit I had a doctor that gave me the doxy as a precaution. The first time I was bit I had a doctor who withheld it.

Having some clue of what can happen to a body that has contracted Lyme’s, I was livid. Fortunately – or unfortunately – I had access to about half a vial of veterinary doxy. See it coming?

Do not try this at home! I took the doggie doxy and apparently took a little too much. Doxycycline produces photosensitivity. I won’t bore you with the chemistry (I researched it at the time), but suffice it to say, the molecular structure of doxy is such that it will store light energy and release it over time. You ‘sunburn’ from the inside out! Don’t need a reference for this. This is personal experience talking. I had second degree sunburn in about a half an hour.

The moral of that story is avoid doggy doxy. Once more I am the star of a cautionary tale. Oy vey!

But the reason I even mention doxy and our conflicted relationship is this: Oracea is doxycycline and it is being researched as treatment for geographic atrophy. There may be hope for my relationship with doxy yet!

According to the good people at Medscape (3/12/17) doxy is being researched as a method of treating low-grade inflammation resulting from alternative complementary pathway activity in geographic atrophy.

The alternative complementary immune system in me is ‘the gang that couldn’t shoot straight’. My good cells are being taken out by ‘friendly fire’. Reducing the effects of the alternative complementary immune system in me would be a good thing. [Lin/Linda: Sue’s referring to what she found out from a genetic test she had. Click here to read more about this.]

The Medscape article veers into uncharted waters for me but I will attempt to translate. It appears doxy can interfere with some of the molecular pathways – read series of actions that are supposed to produce something – that end up creating the conditions that lead to geographic atrophy. It lists oxygen species, matrix metalloproteinase, caspase activation, cytokine production and complement activation. Oh, good grief! Social scientist here! Never took biochemistry.

According to Wikipedia, reactive oxygen species are a normal byproduct of the metabolism of oxygen. In times of environmental stress on the cells, levels can build. It ties in with oxidative stress.

Matrix metalloproteinase are enzymes that break down matrix proteins (don’t ask because I don’t know!). Caspases are enzymes having to do with programmed cell death and cytokines are used by cells to send messages to other cells.

Did I mention I am not a biochemist? Don’t understand it except to say it all – magically! – has something to do with causing divots in maculas. Doxy is supposed to, maybe, could be, slow it down.

Clinical trials of doxycycline – under the brand name of Oracea – are underway. Check clinicaltrials.gov for locations near you. I doubt they would give you too much, but just the same, try to stay out of the sun! Continue reading “Biochemistry Redux”

Do As I Say

Happy Saturday! Welcome to Presidents’ Day weekend! (In real-time, of course.)

I had a nice, long conversation with a representative of the International Macular and Retinal Foundation (IMRF) last evening. (Based in Maine. With a name like that you would think London, Paris, Zurich.) They came upon this website and liked it! (Flattery may not get you everywhere with me, but….OK, so I’m an attention junkie; OK??) Thank you IMRF.

The IMRF publishes self-monitoring tools under the name KeepSight. They sent me a cute, little booklet with basic AMD information, puzzles and different monitoring grids. They are free. IMRF is hoping to spread them around to not only us AMD types but also to doctors’ offices and other places people at risk may congregate. What they are trying to do is stop the progress of dry to wet before severe damage is done.

OK. Let’s stop here for a second. Don’t freak out. According to Bright Focus, only 15% or so of us with dry progress to wet. Lin just wrote a piece on the two types of advanced AMD. They are wet and GA, geographic atrophy. The second one is me; remember? I just got moved to appointments every six months because with my level of macula loss through GA, my chances of changing to wet are slim. Thank God. The more severe damage is done in wet.

Anyway, in the interest of full disclosure – in other words, I can’t lie to save my life so I stopped trying! – I admit I am not big on self-monitoring. My chances of progressing to wet are slim and I am, by nature, a bit of a rebel. However, that is not going to keep me from pulling the old “do as I say, not as I do!” trick on you.

Most of you have a fair amount of macula left and are in the earlier stages of the disease. Do you know you are not going to be part of the 15% that goes wet? I sure don’t. Which means you should self-monitor your vision.

Mayo Clinic gives the following symptoms for wet AMD and an eye bleed:

  • Unusual distortions – that means the wiggles and things with the tops cut off and moved over
  • Reduced central vision
  • Decreased intensity and brightness of colors
  • A well-defined blurry or blind spot in your visual field
  • A general haziness of vision
  • And the important one: Abrupt onset and rapid worsening of symptoms.

In geographic atrophy my macula has been slowly deteriorating. The two times I had a rapid decline in vision scared the daylights out of me and sent me off to the retinologist the same day. If you have a rapid decrease in vision, you should do the same.

The KeepSight booklet has some nice grids and examples of what a problem may look like. If you can’t get a hold of one of their booklets, at least print off a copy of the Amsler Grid and tack it on the fridge. Then use it! Remember, do as I say, not as I do! Continue reading “Do As I Say”

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”

Highlight: Here’s a GREAT website especially for those with wet AMD

Lin/Linda here: Every once in a while I find a website and/or Facebook page that stands out.  Here’s one of those.

The website and Facebook page are called The Science of AMD: Our vision is to save your vision.  It is presented by the Amgiogenesis Foundation. Their headquarters are in Cambridge, Massachusetts.

Click here to go to the website. From there, you can connect to Facebook, Twitter or YouTube using icons in the upper right corner.

What is angiogenesis? From the website: “Angiogenesis is the process used by the body to grow blood vessels. In healthy adults, normal angiogenesis occurs in healing wounds and reproduction, but in all other situations, it is abnormal.”

It’s what causes wet AMD: “Wet AMD is caused by abnormal angiogenesis, when new vessels grow under the macula, disrupting the central region of the retina. These new blood vessels bleed and leak fluid, causing the macula to bulge or lift up from its normally flat position, impairing central vision. If left untreated, scar tissue can form, and central vision is irreversibly lost.” 

What’s so special about the website?
  • From a design standpoint, you can change the size of the font and the color of the font & background, you can choose a version of the site in any of 7 languages as depicted by flags, it’s easy to navigate.
  • Format of content includes printed text, videos, audio, graphics, PDF files and more.
  • This is not just for the US, there are resources available for other countries as well.
What information can I find there?

There’s a menu with Learn, Treat, Resources, Connect, About, Donate.  I suggest you start at Learn!   The emphasis is on how angiogenesis causes wet AMD and what can be done to treat it.

OK, now go and explore! Let me know what you think!

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”

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Highlight: Does wet AMD start as dry?

There are differing opinions and interpretations of what those in the field of macular degeneration have learned.  The links below certainly don’t represent all views, of course, but are an example of some of what you will find.

The important point is that it is CRITICAL to get your eyes examined as recommended by your doctor and to monitor your vision between exams. Click here to find out how to do that.

From: http://www.webrn-maculardegeneration.com/macular-degeneration-stages.html

“Advanced AMD is either a break-down of light sensitive cells and supporting tissue in the central retinal area (advanced dry form), or the development of abnormal and fragile blood vessels under the retina (wet form).”

From: https://www.macular.org/dry-vs-wet-macular-degeneration

“About ten percent of all cases of Age-related Macular Degeneration become “Wet” AMD (typically a person has dry AMD first and progresses toward wet).”

From: https://nei.nih.gov/health/maculardegen/armd_facts

“There are three stages of AMD defined in part by the size and number of drusen under the retina. It is possible to have AMD in one eye only, or to have one eye with a later stage of AMD than the other.

Early AMD. Early AMD is diagnosed by the presence of medium-sized drusen, which are about the width of an average human hair. People with early AMD typically do not have vision loss.

Intermediate AMD. People with intermediate AMD typically have large drusen, pigment changes in the retina, or both. Again, these changes can only be detected during an eye exam. Intermediate AMD may cause some vision loss, but most people will not experience any symptoms.

Late AMD. In addition to drusen, people with late AMD have vision loss from damage to the macula. There are two types of late AMD:

In geographic atrophy (also called dry AMD), there is a gradual breakdown of the light-sensitive cells in the macula that convey visual information to the brain, and of the supporting tissue beneath the macula. These changes cause vision loss.

In neovascular AMD (also called wet AMD), abnormal blood vessels grow underneath the retina. (“Neovascular” literally means “new vessels.”) These vessels can leak fluid and blood, which may lead to swelling and damage of the macula. The damage may be rapid and severe, unlike the more gradual course of geographic atrophy. It is possible to have both geographic atrophy and neovascular AMD in the same eye, and either condition can appear first.”

From: http://www.avruc.com/macular-degeneration.php

“The macula is the central part of the retina and allows us to read fine print clearly and see colors vividly. It is this area of the retina that deteriorates in ARMD. There are 2 forms of ARMD. Everyone who has macular degeneration starts out with the dry type and 20% progress to the wet type over the course of a lifetime. “

From: http://www.youreyes.org/eyehealth/macular-degeneration

“Can the dry form turn into the wet form?
Yes. All people who had wet form AMD had the dry form first. 

The dry form can advance and cause vision loss without turning into the wet form. The dry form also can suddenly turn into the wet form, even during early stage AMD. There is no way to tell if or when the dry form will turn into the wet form.

Can advanced AMD be either the dry form or the wet form?
Yes. Both the wet form and the advanced dry form are considered advanced AMD. Vision loss occurs with either form. In most cases, only advanced AMD can cause vision loss. 

People who have advanced AMD in one eye are at especially high risk of developing advanced AMD in the other eye.”

Please see your doctor for regular exams and between exams, check your vision at home.

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