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Welcome to the Healthy Brain Toolbox. I'm Dr. Ken Sharlin, neurologist, speaker, author, and host for this show. In each episode, I interview influential people whose work impacts how we live and how we think. My guests are leaders in the health and fitness industry, physicians, scientists. Here, you'll find conversations that break down barriers, expand your horizons, and give you the tools you need to protect your health and nourish your aging brain.

Dr. Ken Sharlin: 0:31

Hello, I have as my guest today, Dr. Rudrani Banik. Dr. Banik is a board certified ophthalmologist, fellowship trained in neuro-ophthalmology and integrative medicine. She is based out of New York City and serves as associate professor of ophthalmology at the Icahn School of Medicine at Mount Sinai. And directs a unique practice that bridges vision, brain health, and lifestyle medicine. Dr. Banik's work expands a full spectrum of eye brain disorders from optic neuropathies, migraine, double vision, macular degeneration, and digital eye strain. She combines surgical and medical treatments with nutrition, lifestyle change, and functional medicine to help patients protect and restore their vision and neurological health. Dr. Banik has authored numerous articles leads clinical trials in neuro-ophthalmology, and has been featured in national media as a thought leader in integrative eyecare. I am honored to have her on the Healthy Brain Toolbox Podcast to explore the future of vision, brain eye connections, and how patients can incorporate the latest science into everyday eye health. So, thank you so much, Dr. Banik, for being part of the Healthy Brain Toolbox.

Dr. Rudrani Banik: 1:56

Thank you so much, Dr. Sharlin, for that kind introduction. It's really an honor to be here.

Dr. Ken Sharlin: 2:02

The podcast itself is a relatively new endeavor. You and I did an interview as part of the Dr. Talks, Parkinson's Solution Summit, and I've been honored to be interviewed by you for your podcast. But what I'm getting at is, as we've gotten started, there's been a big focus on emerging technologies, precision medicine, all kinds of really cutting edge things. So I'm looking forward to continuing on that theme and really focusing on some of the most exciting things that have emerged and eye health and the treatment of illnesses affecting vision in the eyes in the last year. It's really been a very exciting year for neuro-ophthalmology and broadly from your perspective, what's making this moment so extraordinary.

Dr. Rudrani Banik: 2:52

I think in the past, neuro-ophthalmology has been a subspecialty of ophthalmology and neurology, but it's been a very reactive field, meaning that we wait for something to happen and then once it happens, we diagnose. And we support, but there really haven't been that many treatment options. And I think this is where the excitement comes in, is that now we're exploring different ways to treat disease using, as you mentioned, some of the latest technologies out there and to restore function. So again, in the past. It's been more supportive care because we didn't have treatment options available and now we have a variety of tools in our toolbox that we can offer patients to try to stabilize their vision problem and perhaps even restore vision that's been lost. So again, it's very exciting.

Dr. Ken Sharlin: 3:44

It really is and we are two sides of the same coin. I have to learn some neuro-ophthalmology, to be a neurologist. Of course, you learn neurology to be a neuro-ophthalmologist. And we share this common ground in that there's an old cliche related to neurology, which was"Diagnose and adios!", Sounds like things are really evolved beyond that now.

Dr. Rudrani Banik: 4:07

Exactly. Yes, same in neurology. It's now a super exciting time in various aspects of neurology and we learned from that as well as neuro ophthalmologists. What is being introduced in mainstream neurology. A lot of those thought processes are now being applied to specific optic nerve diseases. Again, really exciting times. Targeted therapies, personalized therapies some of which are. Based on genetics. Some of them, some of which are based on nutrition and lifestyle. So again it's a wonderful time in our field.

Dr. Ken Sharlin: 4:39

That's excellent.

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Dr. Ken Sharlin: 6:33

Let's dive right in then and if it's okay, let's start with gene therapies. So we've all seen the headlines, children Blind from birth. Now recognizing their parents' faces after a single treatment. It sounds like a miracle but it's built on decades of work decoding the genetics of sight. And I'm wondering, how does gene therapy actually work to restore vision?

Dr. Rudrani Banik: 6:59

You know the eye is a small, complex organ. There's the cornea, the lens, the retina, the optic nerve, and. In some conditions, for example, in some congenital conditions, there are very specific genetic mutations that may affect the retina, for example, and cause vision loss, vision impairment, and even blindness. There's a particular condition called Leber's Congenital Amaurosis or LCA, in which there is a very specific genetic defect. And the way this has evolved is that it's really fascinating technology gene therapy for this condition, LCA whereby a viral vector is introduced into the eye carrying the healthy gene. It's an injection into the eye. And that thought is that the healthy gene would get incorporated into the cells that are carrying the mutant ineffective gene. And the healthy gene would then replace those dysfunctional genes and enable a person to see. So this was the first FDA approved gene therapy in ophthalmology for Leber's congenital amaurosis. Now since then there have been other conditions, in which there are very specific genetic mutations in which gene therapy has been used. And the one that I deal most commonly with is also a Leber's type of problem. The same I believe he was a, an ophthalmologist. I don't quite remember whether he was an ophthalmologist, maybe he was a neurologist. But Dr. Leber had many things named after him. So the condition that I treat very commonly is Leber's hereditary optic neuropathy. So again, there's Leber's congenital amaurosis, and then there's Leber's hereditary optic neuropathy, also known as LHON. And I've been fortunate enough to be involved in a few clinical trials now in which we're using gene therapy. To target a specific genetic mutation in the mitochondrial genome which happens to be passed along through the maternal line. So our mitochondria, we get solely from our mothers, and so it can be passed from generations along the maternal side of the family. And this condition, LHON tends to affect and we quite don't quite understand why this is, tends to affect. Young people and mainly males. So again, it's mitochondrial affects young people between the ages of, let's say 15 to 30 or 35, mainly males. And they lose vision. And usually it's one eye and then the other eye a few weeks to a few months later. And these unfortunate individuals go blind. They're legally blind because of this genetic mutation. And so the gene therapy is designed to. Again, replace the faulty gene mutation in the mitochondrial genome in a specific location called ND four with the correct. In some of the trials that have been performed both it's multinational trials, so here in the US as well as some other nations in Europe we've seen some incredible success with helping people actually regain their vision. After being legally blind. And we're still in the process of getting FDA approvals. There's one more trial that needs to be done. Hopefully in the upcoming year we'll be doing that trial and then hopefully in a few years this treatment is available and commercially available for people with this particular problem.

Dr. Ken Sharlin: 10:30

I'm just curious, I wanna break down a little bit about how this actually works and I hear terms like viral vector and CRISPR and even something called antisense oligonucleotide therapy. And I wonder for our listeners or viewers who could explain a little bit of that so you get a better idea of how this treatment actually improves vision.

Dr. Rudrani Banik: 10:55

Sure. So we are using a viral vector. It's an adenovirus, which is the same species or strains as what typically causes the common cold. But that adenovirus, genetic material the pathogen genetic portions of it are removed, and then the gene that is the correct gene for Leber's, hereditary optic neuropathy gets inserted into the virus. It gets injected into the eye. So this is something called an intravitreal injection. So it's done under local anesthesia. It's done in the doctor's office, not in the operating room, but just in the doctor's office. So an injection goes into the eye after numbing with this viral vector, and so the virus carries the healthy gene, releases it into the back part of the eye. And the thought is that these healthy, the correct gene would then be incorporated into retinal cells because the virus is infecting those retinal cells and it's like Im imbuing the retinal cell with the correct gene. And so that's the thought Now. The truth is that's all hypothesis. Even the company that is sponsoring these trials they still don't exactly know which retinal cells are picking up the genetic material. But we know that yes the virus is in the retina. We've been able to identify it. Interestingly, not in only in the eye that's injected, but also in the other eye is being some transfer of the healthy genetic material via this viral vector from one eye to the other, and so there's a benefit there as well. Now with respect to CRISPR and anti oligo. I don't even remember all the terms but basically those are ways to target the correct genetic sequence. The virus is able to find exactly where the problem is with this technology, and again, I'm not an expert in all of this specific genetics, the technology behind it, but there is a targeting like a marker that the virus is looking for, and then it attaches to that, and then it's inserting the correct gene.

Dr. Ken Sharlin: 13:00

Really exciting. I think that this antisense oligonucleotide therapy this is something that has made its way into mainstream community neurology in the sense that the studies are done. The FDA has stamped its approval for a specific form of ALS or Lou Gehrig's disease. The familial ALS that is triggered by a mutation in the superoxide dismutase one gene. And then I believe there's also a therapy currently commercially available. I have not used it but for spinal muscular atrophy. Which of course overlaps quite a bit in a sense with ALS. So it is exciting. These treatments of course are not without risk. And I suppose one question that folks might want to ask is, Hey you're putting a virus in my eyes. Is that gonna make me sick?

Dr. Rudrani Banik: 13:57

So interestingly, it does not make people sick. So they don't get the common cold, for example, which is typically associated with adenovirus. What they do get sometimes is inflammation in the eye. And so the eye is what we call an immunoprivileged site. So really it's typically not exposed to the immune system. And there is something called the blood retinal barrier. So that's keeping certain cells out of the eye to protect it. But when the virus is injected, it can cause a lot of inflammation. So we have seen that, but it's something that is usually mild and very treatable. So sometimes we do treat people with oral or topical steroids to manage that inflammation. Usually it resolves without any long-term consequences, but no, people typically don't systemically get sick from this virus being injected into them.

Dr. Ken Sharlin: 14:52

Very good. Now, something that I often encounter, I'm sure you do as well, just in Alzheimer's disease alone, for example, in the past year. There's a paper I should say, that comes out every year. It's updated by Jeffrey Cummings reviewing the Alzheimer's Disease Pipeline, and I think in this past year it was 189. Ongoing trials in different phases, looking at something like 130 some odd unique, you know, treatment strategies. And these complicated ideas for a lot of people to wrap their heads around. And I think you've alluded to it but what I'm often asked is, there's one treatment. That gets into the news. It's not, may not even be a treatment. It's a successful experiment in the laboratory on mice. And of course there're those splashy headlines, we finally found the cure and this and that and then I get a hundred phone calls, can I get that treatment right? And it is important for folks to understand that. There is a sequence, there is a way that things come to market. And even in late stage trials, there's an astonishing number of trials that either fail or they some adverse effect comes up that wasn't seen in an ear, as an early signal and phase one or two trials. And so ultimately that treatment can't come to market because of risks. So I know that. We're not necessarily talking about extremely common disorders when we talk about the various labor optic neuropathy disorders. But nevertheless, if you're affected, you're gonna be really keyed in on this information. I want this, i'm gonna call my ophthalmologist. What are your thoughts about how soon we might see some of these treatments in the marketplace?

Dr. Rudrani Banik: 16:39

So this particular treatment is pretty far along. And again, there's one more clinical trial that the FDA mandates has to be done really to see if both eyes need to be injected or just one eye needs to be injected to get the benefit in both eyes. So my guess is that trial would probably take about. Two to three years to complete, and then the data analyzed, presented to the FDA. So I would say probably in the next 5 to 7, on the tail end of it, maybe 10 years, 5 to 10 years, I would say that this may be FDA approved. And I just wanna just address one of the points you mentioned Dr. Sharlin is. A lot of these conditions that affect either the eye or the brain. It's not just a single gene, single solution. And I think people just need to keep that in mind. Some of these conditions are what we call polygenic, meaning that, there's one particular mutation, but then it's other things piled onto it or other risk factors added onto it. One other condition that is very common kind of. The equivalent of Alzheimer's and ophthalmology is macular degeneration. And yes, we've identified many genes. Over 50 genes have been identified, linked to macular degeneration. Just because you have maybe one or more of those genes does not mean that you're going to get the disease. But yes, the genes may play a role and it's not just treating that one gene that ultimately may fix the problem, it's finding a solution that addresses multiple aspects of the disease. So it's not. In all cases a simple fix like the scenario I described, because that's again, a single mutation, single problem, single solution. Some of these conditions are broader and they also present differently in different people. So you can have people with identical genetic makeups, like for example, identical twins, and they may have diseases that present in very different ways based on other things like environment. Give you another example related to macular degeneration. There was a study done in identical twins with macular degeneration in which one twin got advanced macular degeneration and the other twin identically. Identical twin did not. And the factor, the differentiating factor here was smoking. So the twin who smoked had over a two times risk of developing vision loss for macular degeneration compared with the twin who did not smoke. So again, same genetics, different phenotypes based off of what else people are exposed to in their environment, their internal environment, and their external environment.

Dr. Ken Sharlin: 19:12

Which I think gives people a lot of hope. It is very similar studies done with multiple sclerosis and identical twins, and something like a. 25, depending on which study, 25 to 30% risk. If one develops MS, that the other will So clearly somewhere around, up 70, 75% is a diet and lifestyle and environment kind of contribution. Which really is exciting. And I think even some of these diseases where we say, we tend to think this is genetic Huntington's disease. If you have the critical number of triple repeats, you'll get Huntington's disease. But on the other hand, one thing as I say is look, the person who has that critical number of triple repeats, they were born with that and although you can develop Huntington's really almost at any age, very tragically to see it in a young person. Of course there are people who really don't show signs until they're much, much older. So what has been happening, for the better part of their life? Leading up to that and this is really about epigenetics, among other things, if we can control the expression, the genes, it almost doesn't really matter that the genes are there at all.

Dr. Rudrani Banik: 20:21

Absolutely, and I'll go back to Leber's hereditary optic neuropathy. There are families in whom, you know, all the siblings have the gene because they have the same mother, yet not all the children develop vision loss. So there are many other factors besides just having the genetic that particular variant.

Dr. Ken Sharlin: 20:40

So this next wave then isn't really just about fixing genes. It could be about replacing what's been lost or even addressing factors that are driving the expression of those genes. Scientists are growing new retinal cells in the labs, really exciting, transplanting them back into patients.

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Dr. Ken Sharlin: 23:00

Can we talk, I wonder if we could talk a little regenerative medicine in cell therapy and how retinal or RPE cell transplants help restore function in macular degeneration?

Dr. Rudrani Banik: 23:11

Sure. A little bit of anatomy here. So the retina is the light sensing tissue in the back of the eye, and it's very thin and it's transparent, but it's complex. It has over nine layers. So there's nine layers in the retina, and there's a layer underneath the retina called the retinal min epithelium. It's a single layer of cells, and these pigmented cells are basically like the waste collectors for the retina. And the retina is just like the brain, highly metabolically active. It's constantly turning over its cell membranes because it's constantly processing light energy. It's using energy, it's creating waste products. So these RPE cells are crucial in the maintenance of the health of the retina. And what happens in macular degeneration is that these cells. The waste collector cells, the RPE cells start to degenerate and you get these deposits formed called drusen, D-R-U-S-E-N, and drusen is the German word for pebble or stone, and it's called that because when we look in the eye, when we examine someone's retina, we can actually see these waste products developing as these yellowish white lick little. Stonelike deposits and we can measure them. We can see them. And they are one of the precursors to having vision loss from macular degeneration. So really I think it's a misnomer. It's called macular degeneration, but it really should be called RPE degeneration. Because without those cells, the macula wouldn't be able to function. So the thought is that if we replace the dysfunctional RPE cells, that perhaps the retina would function better and not undergo. Vision loss not go down that cascade of oxidative stress and mitochondrial dysfunction and inflammation that ultimately leads to new blood vessels forming that leads to vision loss. There's a sequence of events here that happens in macular degeneration. It's not just something that happens overnight. This probably takes place over years to decades. This whole domino effect, RPE, cell dysfunction, mitochondrial dysfunction, oxidative stress. Inflammation and then new blood vessel growth. So the thought is, could we replace the dysfunctional RPE cells? And yes, there have been trials, some studies done looking at animal models first to try to replace those RPE cells to maybe to do a transplant or maybe. Put healthy RPE cells into the back of the eye. That is a little tricky if you just inject them because they don't necessarily get to where they need to be. They need to be underneath the retina. Technically speaking, it is a bit tricky to do. But that could be ultimately really the way that we treat macular degeneration or prevent it from progressing. Now, currently, the treatments that we have available are aimed at the end stage of the disease. Basically, if someone's already had vision loss. Either from wet macular degeneration where there's bleeding in the back of the eye from these new blood vessels or advanced dry macular degeneration. It's called geographic atrophy. And perhaps you've seen television commercials about this because now these drugs are on the market. They're being promoted to the public through TV ads, but but the current therapies are injections of. Various types of molecules and compounds into the eye to prevent bleeding or prevent inflammation. And so that's the current treatment, but that is, again, reactive to what's already happened. So the thought is if we could catch the disease earlier in its stage before it goes down this pathway and replace the RPE cells, that may be the better way to approach it. I think we're a little far from that though. I'm not sure what the timeline would be, but again, I would probably say 5 to 10 years maybe.

Dr. Ken Sharlin: 27:06

That's super interesting because and if I've understood you correctly, and I'm thinking again about Alzheimer's disease and the currently approved drugs that are disease modifying, the NanoMab and Lecanemab, they have a modest impact on disease trajectory slowing progression by about 27% over 18 months. But on the other hand as you're pointing out and the analogy that I'm making is that these drugs target the amyloid protein or the proto fibrils in the case of Lecanumab. But these are very end stage expressions of Alzheimer's. And of course the goal is to identify the changes even earlier. And not surprisingly, removing the amyloid has limited, it has value, but it has limited value compared to what we could be potentially doing if we identify those earlier drivers of the disease.

Dr. Rudrani Banik: 27:58

Absolutely. And similar to Alzheimer's, addressing the drivers of disease early is so important for macular degeneration as well. Diet. And I'll share with you this really surprising, statistic this study was published actually back in 1994 by one of the leading researchers in macular degeneration, Johanna Seddon. And what she found was that people who have a diet that's rich in the two eye nutrients that are really important for macular degeneration, call lutein and zeaxanthin if you're in the highest. Intake level of these two nutrients, you have a 43% reduced risk of developing vision loss for macular degeneration. Regardless of your genetics, regardless of everything else, just eating some of these nutrients will decrease your risk by 43%, which is mind-boggling. That's better than any statistic from using any drug at the end stage of the disease, which by the way, doesn't recover vision. It just prevents progression of vision loss. So it's not that people who are getting these injections on a monthly basis or every three months are actually getting their vision back. Many of them are not getting their vision back. They're just stabilized where they're at. But why not address it much earlier? And I think this is where you and I are in the same mindset. Using an integrative functional medicine strategy is so important in some of these neurodegenerative conditions.

Dr. Ken Sharlin: 29:23

Yeah, and you brought something up. And again I just I could be completely off base on this, but I always see analogies and connections and you mentioned that drusen and drusen is a term that I often see, when I've either have a consult from an ophthalmologist. Often it's for a condition that you're well aware of called idiopathic intracranial hypertension where someone has looked in the patient's eye, it may even be an optometrist, and there's a, gosh, those optic nerve heads really looks swollen. And then sometimes the ophthalmologist takes a look and goes, ah, that's just drusen. It's not a swollen optic nerve. And again, I could be wrong, so I'm looking forward to getting educated, but you've opened my mind up to this idea because a common report in a brain MRI, as and I'm sure you've seen plenty of reports, probably thousands, where the radiologist says, non-specific, microvascular disease, blah, blah, blah. And we have to explain to our patients what the radiologist's really saying. And the temptation is to say, oh, this is just normal wear and tear of aging. It's not really a diagnosis, it's not really a sign of a diagnosable illness. But in reality, you know what I tell my patients? Look, first of all we do know that overall the greater burden of these white matter changes is microvascular disease. The greater likelihood that you'll develop. Alzheimer's or some other form of dementia, stroke, or even have premature death. And we do need to look at it as a reflection of the overall health of the brain, of the person whose brain that is, right? Do they have high blood pressure? Do they have dyslipidemia? Are they insulin resistant? All the things that lead to that premature wear and tear. So it sounds like this sort of drusen where oh, it's not a swollen optic nerve, it's just some drusen. Maybe I should be more cognizant of that.

Dr. Rudrani Banik: 31:25

Yeah, that's a great point, Dr. Sharlin. I do wanna differentiate something though, again, in ophthalmology, we for good or bad, we use the same term for different things. So just like we use Leber's for different conditions, we use drusen for different conditions. So there's drusen in the macula, which are these kind of yellowish, white pebble looking deposits, and there's drusen of the optic nerve, which are lumpy, bumpy, yellowish, white deposits. And they're different. They're different and their locations are different. So the drusen that you're referring to underneath the optic nerve, on the surface of the optic nerve are actually quite common. They're present in 1 to 2% of the normal population, and it is an autosomal dominant trait to have these drusen optic disc drusen and they're really like extracellular deposits, calcium mainly but extracellular calcium and hyaline deposits along the optic nerve. And yes, they can make the nerve look swollen. Sometimes they can even cause peripheral vision loss. So this why at the ophthalmologist's office, if you've been diagnosed with drusen optic disc drusen, you will get a visual field for baseline. That's what we do. And in many cases they're benign, but sometimes again, they can cause some degree of vision loss or peripheral vision loss and yes, could it be something, you know what, to your point earlier about some of these, markers that we sometimes just disregard oh, it's nothing. Could it be reflective of some alteration in metabolism that's causing these types of things to develop drusen or these non-specific white matter changes, which by the way, I've had brain MRIs and I have one or two of those non-specific white matter changes in my brain. I also have migraines, so I'm chalking it up to my migraine, why I have those but they're quite common. And could they be reflective of something else going on metabolically that may be a precursor we don't yet know with Drusen. But as far as, if someone has drusen, I think what your point was like to tell the difference. Is it just drusen making the nerve look swollen or is it really swollen? A condition that we call papilledema from idiopathic intracranial hypertension or IIH which is high pressure in the brain.

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Dr. Ken Sharlin: 35:20

Yeah. Yeah. Before we go on to the next subject, I wanted to share some of these, it speaks to your comments about addressing the root causes of macular degeneration. I have a colleague who developed. Was developing macular degeneration. Still fairly early stage, but concerning enough went to see another mutual colleague of ours who offers a procedure that, to my knowledge, it's perfectly, quote, legal to do it, but it's not a broadly FDA approved called therapeutic plasma exchange. And then much of this comes out of some of the research looking at and this is lab research of. When an old mouse and a young mouse, or have their circulatory systems, sewn together, the young mouse gets old and the old mouse gets young and we think that there are various, things in the blood that drive that biological aging process, whether it's driving inflammation, oxidative stress, epigenetic signals, what genes are turned on and what genes are turned off. And then this has been translated into therapeutic plasma exchange. And although I don't know that we could accurately say cure. This dear colleague of mine went back to her ophthalmologist and so far she's in remission and I just wonder if you've seen any of that? That's pretty incredible.

Dr. Rudrani Banik: 36:44

Yeah, that's a fascinating concept. And actually one of my retina colleagues just the other day was asked me about therapeutic plasma exchange and my experience with it. So the thought is that by exchanging one's plasma, you are removing particularly inflammatory cells or immunoglobulins or complement proteins from the blood that may be propagating inflammation. And we know that in macular degeneration, there is definitely a cascade of inflammation that happens as one of those dominoes that are falling before vision loss occurs. And we know that the complement system is involved. We still don't quite understand the details of this, but the thought, again, to your story of your N-of-1 case, it's possible that through this therapeutic plasma exchange that enough of those inflammatory mediators were removed from this person's. System to allow the inflammation and the retina to calm down. So I am fascinated by this. I would love to learn more about it and see, how it may potentially benefit my patients. One other thing that is really really cutting edge, you are asking Dr. Sharlin about what's new and exciting in ophthalmology. One thing I wanted to share is photobiomodulation. Yes, and I know that it's really gotten a lot of light therapy. Basically red and infrared light therapy has gotten so much positive attention for other types of conditions, whether that be dermatologic conditions, wound healing arthritis etcetera. I'm not sure even about brain health. If there are any studies. Probably there have been cognitive studies done. So there is a recent FDA approval that really warrants a lot of attention. And this is a light therapy device, again, called photobiomodulation for macular degeneration and this particular device is called the Valeda device, is the trait like commercial name for it and it is now available in some retina doctor's offices. And what it does is it basically delivers specific wavelengths, three different types of wavelengths to the eye, so it develops red light. At 660 nanometers infrared light at 850 nanometers and yellow or amber light at 590 nanometers, and it develop, delivers it in pulses. So it's about a three minute course of therapy per eye, and it's giving you a various like pre-programmed number of pulses to the eyes. Some of it is done with the eyes open and other parts are done with the eyes closed. Now this is very exciting because the clinical trials showed, and the clinical trials again led to that we know, number one, it's safe. It's a safe therapy to use really no adverse events that were serious and we know that it works. So in patients with dry macular degeneration, the light therapy help them regain. Please don't quote me on this, but I wanna say the equivalent of about two lines on the chart, which is fascinating that this light therapy, it's given for nine sessions over three to four weeks, and again, it's three minutes per eye, so it doesn't take that long and there's really no downtime. But it's something that I think is really a huge. Milestone in the use of these types of really advanced technologies. But that goes back to ancient thinking that, we can use light in various ways to help our bodies heal and we use light from the sun. Now we have these artificial sources of light, it has a tremendous regenerative capability. And so again, it's FDA approved for macular degeneration, dry macular degeneration, and they've also done studies in glaucoma. So in the future it may be also approved for glaucoma and I'm really looking forward to it also being approved for other optic neuropathies, including LHON as well. So there are a lot of different types of applications for which this light therapy may be beneficial.

Dr. Ken Sharlin: 40:48

Absolutely exciting stuff. I wanna encourage listeners who wanna learn more broadly, learn more about photobiomodulation. We have a wonderful podcast interview with Jordan Hamlin from Neuronic, and that's near infrared photobiomodulation on the brain and we're talking about how light can be used to heal the eyes. So, great stuff. Definitely one of those we'd say is a subject for a whole other podcast for sure. But also wonderful transition into talking about technology, AI, robotics, long-acting, delivery robotics systems have found their way into ophthalmology and transforming, precision. The precision of gene and cell delivery. Long-acting implants various other technologies. I wonder if we can explore some of that.

Dr. Rudrani Banik: 41:37

Absolutely. So robotic eye surgery is happening at my institution, which is again Mount Sinai at here in New York City. I have a colleague who's done a lot of research in using robotic surgery for glaucoma surgery, for example. We're also using it potentially for in the future cataract surgery. So I think these ultimately will become mainstream, these types of approaches. Of course, they do require experienced surgeons to operate the technology, the robotics. But remember the eye is so small and it's so delicate. And so the precision that's required to get to the area that we want to target, that we want to operate on has to be, it's in the level of micrometers. That's how small we need to get. So again, this is evolving technology but it's already being done, some of it's a work in progress to explain a little bit more about some of the drug delivery systems that you were sharing. I recently went to our annual ophthalmology conference, and I learned of this tiny little implant that can be given into the eye that will release sustained anti-VEGF. And this is a treatment for macular degeneration, so you can get a tiny little implant put in. And then after the implant is put in surgically, you can have it refilled, the chamber refilled, and I don't remember exactly how often. I think it's every six months that it needs to be refilled with the drug. So it's not going back to the operating room every single time, but you get the implant put in and then you can have it refilled periodically. So it provides durable, long lasting relief rather than going to the eye doctor once a month to get a monthly injection, which can be very uncomfortable.

Dr. Ken Sharlin: 43:22

So that's vascular endothelial growth factor. And if I'm following this, the logic here you distinguish between wet and dry macular degeneration. I'm assuming that the folks with the wet macular degeneration would particularly benefit from that.

Dr. Rudrani Banik: 43:39

It is for wet only at this point. Yes, because it's anti-VEGF as you mentioned, vascular endothelial growth factor. And you would think that, oh, it's a good thing if blood vessels are growing in the eye, there's more oxygen, there's more blood flow. But these blood vessels that grow are secondary to inflammation and they're not normal blood vessels. They're very fine capillaries and they bleed very easily. And we want them not to grow. We want them to get absorbed and basically not be a risk to the eye. So these drugs basically block that cascade. The factor that kind of causes the blood vessels to grow is blocked. And I'm simplifying obviously but that's the thought with using these anti-VEGF treatments in the eye.

Dr. Ken Sharlin: 44:23

That is really cool. And another area that affects all of us, all the way down to the everyday person, the consumer various section, business that has nothing to do with medicine, but of course me in neurology, ophthalmology is artificial intelligence, right? We are just at the beginning of what AI can do and I'm wondering from your vantage point what are you seeing with AI? Helping doctors to detect diseases earlier or predict who's gonna lose their vision.

Dr. Rudrani Banik: 44:52

Oh, this is a really, a burgeoning field in ophthalmology is the use of AI and technology. First of all, there are. Are wide areas, both in the United States as well as in other parts of the world where care is not accessible to eye doctors. There aren't that many eye doctors in the area, so people don't typically go and get their routine exams, et cetera. So there is technology whereby there are cameras. That can take a photograph of the retina and the optic nerve, and that can do that, through a non dilated exam. So typically we put drops in the eyes to dilate the pupil so we can check the retina. This is a way to do it in which no drops are required. A photograph is taken and then analyzed using AI, where they have a database of probably hundreds of thousands of individuals, both normals as well as people who have pathology. And they can be screened for things like diabetic retinopathy, for macular degeneration, for glaucoma, for other optic nerve issues. So a wide variety of screening algorithms are being developed so that this. It can be delivered. This care can be delivered through telehealth, basically. So you can go see maybe your primary eye sorry. Primary care doctor, if they happen to have one of these cameras in the future, they take a picture, they have AI, analyze it, and if anything gets flagged, then that patient is then referred to an eye doctor, an ophthalmologist, that's just one example whereby eyecare may be more accessible to individuals wide, again, wide populations of individuals and screening can be so much more effective and economical for patients.

Dr. Ken Sharlin: 46:35

That's great. If we step back at this, what we are witnessing is medicine evolving from managing decline to restoring possibility, right? Whether it's vision, whether it's brain function overall. In the past two years, we've seen repair, gene repair, stem cell replacement, mitochondrial rescue, AI diagnostics with each piece, bringing us closer dream of curing blindness. That's amazing. And I'm wondering, when you look across all these breakthroughs, what do you think curing blindness will mean really in the next decade?

Dr. Rudrani Banik: 47:13

So I think in the next decade, realistically, for people who are severely visually impaired, there will be ways to allow them to see, to some degree, perhaps not normal, but to some degree to allow them to regain some function in their life, maybe some independence, navigation, perhaps even being able to read, not to say that they'll be able to see 2020, but some degree of functional vision, and that's the goal. And now whether that be through some of the modalities we talked about, whether that be through gene therapy for specific mutations, genetic mutations, whether it be through photobiomodulation, whether it be through optogenetics, which we didn't touch that much upon, but that's another field that's very exciting in ophthalmology and whether that be through some of these new drug delivery systems, I think that probably people who previously really we did not have much to offer them, we will now have more tools in our toolbox to share with them to help them lead more functional lives. And just a word about technology I recently came across. There are all these smart glasses out there including meta, meta glasses by RayBan. I actually demoed them and it's pretty remarkable what they can do. For people who have vision impairment they can read something for you and verbally tell you what there, let's say it's a sign, a street sign, et cetera. They can identify colors and obstacles and improve safety. So aside from the vision aspect, there's other ways that technology can help people who have vision impairment. And I think we really need to dive into that, especially as eye care providers. A lot of my colleagues and I really aren't aware of some of these technologies, and I really wish that more people would be open to it and try to learn more because then we can better serve our patients.

Dr. Ken Sharlin: 49:07

So true. Dr. Banik, as we round out our interview today, what message would you share with patients or families been told there's no hope for their vision?

Dr. Rudrani Banik: 49:19

I would say there is hope. There is always hope and I think it's really important if you have a provider that you're working with and they're telling you, there's nothing more we can do. Please be your own advocate and do your own research and find what's out there. Now, with a grain of salt, you want to go to trusted sites. If you see another provider, make sure that they're doing something. If they're doing any kind of experimental therapy, make sure it's under the auspices of a clinical trial to make sure that it's safe. That's number one, is safety. To make sure that whatever new technology is being used is not gonna cause any harm, but do your research. There's so much available now on the internet for us to learn and explore. Find ways that you may be able to participate in a clinical trial or or find a provider who can help get you the help that you need.

Dr. Ken Sharlin: 50:12

Wonderful. Dr. Barnik, if folks wanna learn more about your work, if they want to connect with you, your clinic, the medical school can you just share with us some ways they can reach out and learn more?

Dr. Rudrani Banik: 50:24

Absolutely. So my website is probably the best way, www.drranibanik.com. And on my website I have links to my podcast. It's called the Eye-Q Podcast. So I interview a lot. I would say leaders in my field and some of the topics that we talked about today. And then also I do similar to your Parkinson's Solutions Summit, Dr. Sharlin, I do have a summit called the Eye Summit that I did last year and I'm gonna be doing it next year as well to bring together information for the public to really see what the latest is out there in terms of new treatment approaches, new technologies.

Dr. Ken Sharlin: 50:58

Very exciting. Folks, this is why I love doing the Healthy Brain Toolbox podcast. We're seeing the boundaries of neurology not ophthalmology and biotechnology really dissolve into a new kind of medicine and one that restores and doesn't just quote, treat My guest today, Dr. Rudrani Banik, a leader in ophthalmology and neuro-ophthalmology, has shared with us some of the most cutting edge, exciting things that have happened in her field in the last year. I hope you've enjoyed the podcast. I look forward to more discussions with Dr. Banik. I just want you to understand that the future of vision isn't about accepting decline. It's about unlocking repair. So thank you so much for joining me, Dr. Banik. Folks, i'm Dr. Ken Sharlin. Stay curious and hopeful and keep building your healthy brain toolbox. Thank you again.

COMMERCIAL BREAK: 51:57

Hi everyone. Dr. Ken Sharlin here with the Healthy Brain Toolbox. I'd love to hear from you. If you have general questions about brain health, neurology, or the science of keeping your brain sharp. Send them to questions@healthybraintoolbox.com. I'll be reading your questions on the upcoming episodes. Please remember, these need to be general questions, can't answer personal medical questions, or provide individual medical advice. So if you've ever wondered about brain health strategies, lifestyle tips, new research, or the future of neuroscience, send those questions in. I look forward to hearing from you and who knows? You might even hear your question featured on the show. Thank you for tuning into the Healthy Brain Toolbox podcast. I hope today's conversation gave you new insights to protect and nourish your brain. Be sure to subscribe, leave a review and share this episode with anyone looking to take control of their health. Until next time, stay sharp and keep learning.