Episode 196 is about an exciting research work on myelin repair in the progressive course of MS with the help of astrocyte cells that contribute to it under administration of Medrysone, a corticosteroid.
My interview guest is Dr. Markley Silva Oliveira Junior, who wrote his doctoral thesis on this topic at Heinrich Heine University in Düsseldorf. It didn’t stop at writing alone, though; Markley did a lot of experimentation and found amazing things about astrocytes, whose impact used to be viewed rather negatively, but which make a crucial contribution to repair.
And since Medrysone is already an approved drug in the field of ophthalmology, it could go faster with the approval, if the successful results from animal experiments, are equally good for humans.
The podcast and blog post are also available in German translation.
Table of Contents
Introduction of Dr. Markley Silva Oliveira-Junior
Hi everyone. Just glad to be here in invitation from Nele, many thanks for having me. Well, I’m a very honored Brazilian guy, neuroscientist, married, I love a good hiking, travelling, good food (quite spoiled I am for being Brazilian, but France and Italy have my heart on that) and of course hangout with my friends and family.
Personal motivation for your career choice
Help people with my knowledge. Being a scientist is actually doing that and I realize this motivation while developing my career. Person who bears a neurodegenerative disease are often exposed to both occasion, illness of the body while self-aware of the whole thing or losing itself while forgot about important things. This is quite sad and being part of those who think and develop solutions for this matter is what makes me happier.
Mechanism of myelin repair in MS-patients
What role does research on remyelination play in the MS research community?
There are several partitions on that area of research basically promotion of remyelination via a plethora of tools. Human stem cell therapy, disease modifying therapies, drug-based therapies and so on. It is quite vast you know.
How easy or hard is it for the central nervous system to repair myelin?
It is simple but not easy. We keep remyelinating the brain while ageing and this is normal, it happens all the time. To form new memories hence synapses or sustain a habit, you need strong synapses and a robust mechanism of electrical communication between neurons and to that to keep happening you do need remyelination to be renovated and sustained over time. Once that memory or habit is no longer needed new synapses are made with the same neurons and again remyelination or myelination is necessary. However during diseases specifically MS, due to inflammation and other discrepancies in the brain metabolism remyelination is weak or not enough to surpass loss of cells for example.
What needs to happen before efficient remyelination can take place?
First of all, reduction of inflammation. We understand that in animals this is an important step to be regulated prior to remyelination to take place. Regulation of oxidative stress, in that case reduction can support a primal recovery of myelin for example, however sustainment in chronification is related to synapse recovery and tissue reconstruction.
How does the ability to remyelinate changes over the lifespan of a person?
There are particularities that just because you are ageing you will face whatsoever. The key one is your glial cells that interact with blood vessels both the astrocytes and microglia, cells that are only in the brain and spinal cord that communicate with your blood that while ageing became as we call reactive, in this case ore sensitive to be pro-inflammatory.
A second thing is that you have a decrease in the expansion capability of neural stem cells at your ventricles and hippocampus and this not only impact the generation of new neurons but also of new oligodendrocytes for example that can be mor efficient than old ones to sustain and generate new memories. Hence, if you are older even though healthy this will happen and if you connect a unhealthy life style lack of sunlight exposure and aerobic activity you have the combo to develop a neurodegenerative disease.
How much is the complex process of remyelination understood so far?
Well not too deep as we wish to be. What we do know is that once demyelination occurs, and an axon is still preserved they express molecules that will induce astrocytes and microglial to call back oligodendrocyte progenitors to this site where demyelination occurred. Once there those OPCs maturate with the support of other mature oligos still in place and also astrocytes more specifically and remyelinate this axon that were once demyelinated.
What cell types play an important role for the remyelination process?
I can list a bunch here, but the key ones are all cells within the brain, including, leucocytes that surround the meninges during inflammation.
How do the different types of astrocytes play a role in repairing myelin?
That is quite an interesting topic because is my key area of research since 2016. Astrocytes are in a glance and inherently heterogenous, this means that they are naturally and plastic cells.
Which special types of astrocytes did you focus on and why?
The ones that I researched in my PHD, for example, were the ones that are responsible for demyelination to occur, hence the loss of myelin and the ones that are probably helping the brain to be recover. So, we actually found 7 different subtypes of astrocytes that are populating the corpus callosum. The corpus callosum is the rich lipid area that we have in our brain that connects both hemispheres, distributing axons forward and backwards in our brain and, up and down, for sure. Throughout this, thanks mostly to the brain, we can… we have axons… that are so big that they go from one hemisphere to another, connecting brains. They emit communication to occur.
What is interesting about the corpus callosum is that we don’t have the body of the neurons there, just these arms, they are so big, maybe legs because they are really big, of access going there. And what was interesting about what we found in my research was this: that we have these 7 different subtypes and some of them are only present during the process of demyelination… so, one thing that I have to emphasize in particular is, I’ve worked with chronic demyelination. In chronic demyelination sometimes you don’t even have leukocyte, or a white cell from the blood inside the brain doing something. You have most likely just the glial cells just interacting with pericytes or a ependymal cells, or other subtypes of cells that we have in the brain. So, the whole mechanism is different.
So, I can’t tell you that there are only those 7 subtypes in chronic, also because I have just been looking into two different parts of the brain. We don’t know how this is, for example, happening in the striatum for example. Which is an area where you have all the dopaminergic neurons. They are the ones who produce a lot of dopamine and make your cortex understand that it is a pleasure to do work and see the result afterwards. Astrocytes are different, so I don’t know if these 7 subtypes that I have found are also in this striatum and if in the acute phase they are also present.
What I know by my work is a really small frame of the whole thing, because we don’t know, actually anything that we have down there, that was happening, is that we have these 7 subtypes. Some of them are present through the demyelination process, or during remyelination process. But we do know is that there is one drug… We can talk about this one in the next questions… that were able to increase these subtypes.
They are actually pro remyelination. There was one of there… cutting edge or nice results that we were able to get. That is a specific drug that can make these cells, that they are pro remyelination, these astrocytes to be increasing and together with this, also remyelination and because they were increasing and remyelination was also occurring, we were able to find that this cells specifically, these 3 subtypes of astrocytes that we have identified, they have molecules, being expressed by them that is nowhere in the literature that is able to make oligodendrocytes to survive, neurons to be regenerated, new neurons to be born, progenitor cells that can turn into neurons, new oligodendrocytes.
That is one molecule in particular, which is called Timp1. And this one is so interesting because is one of the few molecules that we know, that when the astrocytes are expressing, they are helping myelin to be recovered. And this molecule was able to increase the expression of these molecules specifically in astrocytes. So this was one of nice and good things that we have found about these different subtypes of astrocytes. around the brain, during chronic remyelination.
What type of experiments did you use?
There’re a lot of things. First we had to develop a model that mimics the chronic demyelination in mice. There is a toxin called cuprizone that is a copper chelator. And as a copper chelator it will mess up everything related to minerals metabolism inside cells.
But one thing about cuprizone which is interesting is they have a tropism for oligodendrocytes cells. It can regulate, actually hyper regulate in a specific pathway that is in relation with inflammation, which is a complement pathway. And when these 2 things are happening oligodendrocytes will die. And this, when oligodendrocytes are dying, is one of the key features of chronic development in multiple sclerosis and together with that you also have the loss of myelin.
If you stand this process, it means you have chronification and what we do with mice is basically extend this time frame of receiving cuprizone and how we do this actually? We have cuprizone in their food. so, in the food we have cuprizone, this toxin and mice will eat this during the research of time of weeks. So, from 9 weeks to 14/34 weeks, feeding mice with cuprizone, they will develop chronic demyelination.
And then we have the other way. To investigate this, we can do a lot of different investigations, but in my case, what I did was investigate in genes, they are related to inflammation, remyelination, demyelination and one process in particular, that we called reactive astrogliosis. Which is a really difficult name to say it, but it’s basically telling the astrocytes be reactive. And by reactive is basically when you have a really bad day in the work, and someone is just horning when you are in traffic, and you’re just upset and any gasoline that will spill up it will turn into fire. And this is how an astrocyte is when it is reactive. He’s already so mad, that anything that goes wrong will make a really big mess. This is how you define as astrocyte is reactive.
And there are certain topics that will make these cells get reactive. And one of those is disease. Why they are getting reactive, we don’t know. And the way that we define to figure out why these cells are reactive was by investigating their gene expression. Which kind of genes are being expressed in the regions of the brain that we have investigated or relating this to astrocytes. And also doing this specific… which is quite a beautiful experiment, that we call immunofluorescence, which is basically making the proteins of these molecules are expressing, glow and take pictures with the microscope.
So you can see the morphology, where they are in the brain and in which protein molecules they are expressing and then you can also quantify these cells. You may get a mouse that is healthy, one that is sick, and you treat one with the drug. You can tell by this technique in the microscope, how many cells are in that area of the brain, enhanced or decreased. If you look into these different groups. And that was basically what we have done in my work, is quantify the numbers of cells in different parts of the brain, if they are going up and down when you treat them with some drugs or when you give them cuprizone and correlate this with disease and also of course, with literature. And then you can tell a story. Sometimes, not a good story, sometimes a good story, but…Yeah.
The effect of corticosteroid medrysone on the myelin repair in MS-patients
Why did you used corticosteroid medrysone in your research? Was there a certain hint, that it might be effective for remyelination?
Well, if we recall about how corticosteroids are addressed to patients with MS most of the time… depends of course on how the doctors are addressing the treatment. It’s basically closer to relapses. So, people that have MS for too long, they, most of the time are not really getting corticosteroids for their treatments. Of course, this can change, depending on the approach of each doctor, but the usual is, patients with chronification of MS are not often getting corticosteroids. So, the first thing was: Let’s try to select a classification of molecules that are no longer being investigated in MS the use of corticosteroid.
Specifically, for chronification corticosteroids. And then we did what we call as pharmacogenomic evaluations, which is basically looking into the pharmacology of this molecule and the genes that are related to this pharmacology effect. And then we looked into this all throughout open libraries which is a huge institute all around the world. They have a data bank of which genes these molecules can upregulate. And then doing investigations in more than 1000 molecules. We get into a list of 5 that were able to upregulate certain genes that we do know that can upregulate myelin and also oligodendrocytes to survive during damage. And 1 of those 5 was medrysone.
So, I investigated those 5 during my PHD and medrysone was the star of the show as I can say. Was the key one, at least with cells, not in animals. We got these cells in a dish, cultured them, took care of them and we could directly see what was going on. With these cells that we have treated with medrysone, we saw it, by doing investigation with a gene expression, there are certain pathways that these molecules can upregulate. They are related with oligodendrocytes maturation and myelination. And medrysone was the best one. I guess I can say it like this. In this field, making this happen. So we decided do make medrysone for those different features that I have explained to you.
What is the effect of corticosteroid medrysone on astrocytes and how does this help with myelin repair?
There are certain receptors in astrocytes, they are related to respond to corticosteroids. One of those is the whole estrogen pathway. Once this pathway is activated in the astrocytes, for example, they can produce molecules that are related to neuroprotection. Brain regeneration, oligodendrocyte replacement, which is basically make an oligodendrocyte to take the place of the one that has died. And those are related to corticosteroid in general. We haven’t actually researched why this specific mechanism regulated by medrysone in astrocytes, but we do know that this cell can make astrocytes be less reactivate. If you remember what I said about reactivity, is basically making these cells to be less toxic. And that we know.
And this is happening because medrysone has decreased the expression of certain genes in these astrocytes. For example, the complement three factor (C3) which is related to enhancement of apoptosis, which is when a cell decides to die to no longer live, is destroyed by this process called apoptosis and medrysone can make astrocytes decrease the expression of C3 in vitro. Which is not in animals. However, in another way, it can also decrease another pathway of Interleukin 6.
You have probably heard about it, has also an important part in MS during the acute phase of MS. Interleukin 6 is decreased, we see less damage in myelin. However in this, we saw the opposite, which was really interesting to see it. Astrocytes, even though you treat the animals with medrysone, they keep expressing C3 and levels of Interleukin 6 are high. So, we started to think “Ok, what’s going on here?” and what we know is that Interleukin 6 during the chronification process, is beneficial to that process to happen.
And astrocytes can express these molecules in higher levels. So, for example, synapses can be redone because of the whole oxidative stress that is going down when you’re having this Interleukin 6 going up. This is the chronification process, not in the innflammatory one that’s there. Both different. And even though animals were treated with medrysone, they were also expressing C3, which is their molecule, that were regulating apoptosis. That we know to be regulating apoptosis. Astrocytes were still expressing, so we started to think “Ok, these cells are a little crazy, maybe.
They express in molecules that we know and the literature, that are not beneficial, but are also expressing in molecules that we know that are beneficial. So they are hybrid. What we do not know is what is going on that they are expressing both molecules, even though they benefit to the problem. And this is how tricky it is for your mind, what is that the medrysone is actually activating or not these cells. We do not know. But we know that these ones that we called hybrid, they express a lot of molecules that are related to protection. Medrysone is enhancing these cells, in astrocytes, specifically. But what specifically, is medrysone doing with these cells, we do not know yet. We’ll hopefully know about this in the near future, but by far, what we do know is that the medrysone can somehow make these cells less reactive and increase in positivity to repair. I guess I can say it like this.
Can you summarize the most important outcome of your research project in Düsseldorf?
First was to show that corticosteroid can do so good, also during chronification, at least in animals. This was quite remarkable of our research. This was the first one to show this chronification process of demyelination. And, to show that astrocytes are also important during the remyelination process, during chronification. Once you regulate these cells, once repair is happening, these cells are also being modulated. They can also express molecules that are known to be beneficial, to myelin to be recovered. Not only to be detrimental, has we once thought a few years ago. Because, back in time, everybody that was talking about astrocytes was always telling look these cells were always reactive and they are there to destroy, we need to remove these cells. And what we do know right now is that, if you remove astrocytes, things will get worse.
So, now, the whole aspect of the research with astrocytes, for example, and microglia is to make these cells healthy again, at least make them get to they fit properly talking and by using medrysone we were able to see that with this corticosteroid we can have two things at the same time, which is super cool. We can have remyelination and also make astrocytes be happy again. At least we expect this to be going forward also in humans … of course, this all data of research in animals but maybe in the near future, in 5 years from now, we’ll be able to see more data come regarding humans in MS and after medrysone, how they are responding to the treatment. Because this will be also different. We cannot say yet that medrysone is the cure for MS. I don’t think that it is, actually. I think there are other approaches, that could be directed to different patients, and we have talked in the beginning right now.
This precision medicine is necessary. There is hope medrysone is really resourcing. molecule that needs attention from the company. Because developing a new drug… and this is actually one the things that is most exciting about my research, is that developing a new drug can take, maybe 17 years and that was something that I haven’t talked here yet, but medrysone was actually not developed to treat MS.
Medrysone was developed to treat eye inflammation, it’s a molecule produced by a pharmaceutical company that is specialized in eye care and it was developed to treat inflammation in the eye or to prevent inflammation after surgery. What we did with medrysone was a drug repurposing. Which is basically getting a drug that was already accepted or authorized by FDA or EMA in Europe to treat a specific disease and repositioning this drug was basically using it in research. So, we can establish a new path so this molecule can be authorized by these federations to be used to treat a specific disease. With MS it’s very important, because when you requisition a drug, you can be way faster than producing a new one. You can save 10, 12 years, by repositioning a drug. So, this was one of the remarkable findings I think about my research in Germany.
You’ve just started a new position as Scientific Consultant at Biolinker a Brazilian Biotech company. What is your focus now?
Now I am focus in neuroscience in my position. So, I’m basically consulting with clients, with professors, physicians or residents that are willing to work with MS, that want to develop in their line of research new biotechnology tools to find new treatments, new models to develop this disease, to then find new drugs or, as we do in our company, develop new proteins and new proteins can also be new drugs.
So, for example, I was talking with a client last week. She’s aiming to produce a vaccine, a kind of medication to treat MS and I am developing, together with her, the whole pipeline to develop getting a drug we can test in the laboratory, to the near future, probably 10 years from now get these molecules in the market to treat MS specifically for atypical MS. Which is when people are diagnosed in the first relapse of their life. Her interest is basically to make these relapses to not happen again. She has already done this in animals, she wants to get into the next level. Produce a molecule that the bio-viability is high, so that’s why I’m working with her as well, so we can produce a molecule to have a high bio-viability because we lost a lot of molecules in this already.
So, we injected… imagine that after injection, just 2.5% of the molecules are getting to the brain. And we don’t want that. We want to develop a mechanism that makes the whole bunch of molecules that we are injecting to go directly to the brain. So, we are trying together with the research and development (R&D) team of our company to develop a mechanism that can deliver this drug more precisely to the brain. We are not actually aiming to do this only… The company that I’m working now, is actually… We are trying to connect with other ones so we can get together and make this happen. So I’m kind of still working with MS. I haven’t really left the academia totally, because I’m still focusing on neuroscience and most of my clients also work with MS and also Parkinson, but most of them with MS.
Who would benefit in the first place from your research? And how far is your research away from first studies with humans?
The whole proposal that we first did in our research was to focus on patients that are in the progressive phase of the disease, which is level of repair and regeneration of myelin is poor, it’s no longer happening as it was before. It’s already slowly happening. The level of degeneration of the brain atrophy is high. So, the focus will be more specifically to those patients. However, how far my research is away from these patients is that basically, I don’t believe that medrysone can be used alone to treat these mice. Because the whole complexity of the disease in terms of inflammation and tissue degeneration is too big for a molecule that is not that strong to make this happen. For example, dexamethasone, which is a different corticosteroid, is 200 times stronger than medrysone in making inflammation to go down.
However, the level of toxicity of dexamethasone can be high for some people, mostly for the liver. So medrysone can be beneficial for this topic, probably for people that have already passed during the primary progressive phase, or secondary progressive phase of MS, taking corticosteroids, medrysone is a little bit less severe and strong than other corticosteroids in terms of intensity, of more co-activation. So, can be better addressed to those patients in the progressive phase. But we are too far from this. This drug can be used off label, which is basically when a doctor is prescribing a drug that was not authorized by these federations to treat altered mind disease. So, this can be done. There are some drugs that doctors recommend to their patients, depending on the prognosis. But I don’t think this will be beneficial if we don’t know much about how these molecules are acting specifically in disease, so I think maybe, a few more years from now, with more research into this topic, can really tell us how beneficial medrysone would be to treat MS. Or, at least, to support treatment with MS, with other molecules such as ocrelizumab, natalizumab and other molecules that we have in the market, they are more specific to treat pre-inflammatory factors.
Because if you think about corticosteroids as a molecule, it’s not specific as these monoclonal antibodies that we have in the market. It’s a molecule that acts in different areas of the inflammation process. Not only one, so I think the most beneficial thing about these molecules, such as corticosteroids, is to be used in combination with other ones. But, of course, this is always a decision of your doctor. I’m not recommending any kind of approach here. Your doctor will always tell you what the best option for your treatment is. In my opinion, maybe, corticosteroids such as medrysone, can be addressed that way.
Can you give us an idea how the expected outcome would look like for people with progressive MS if the treatment would work at one point? What do you know from the mice models?
We have not published this data, but we have evaluated where mice were developing, after direct treatment. How they were behaving. Where we were able to see if they are completely normal? They get normal again. However, there’s something I need to tell you. Basically, on my model, what we do know is that, even if you don’t give a drug to these mice, a few weeks later, after eating cuprizone they will get better. However, there is a small time, sometimes 3 to 4 weeks, where these mice are really sick. We took cuprizone from their diet but are still sick.
However, when before removing cuprizone from their diet, we gave them medrysone, they got healthy way faster, then if they weren’t receiving the molecule. So, if we took only this time frame, where this animal is still passing through the relapsing time, he’s still recovering from the recent damage of the myelin that he had; if we look into medrysone we would say “wow, this molecule is really making these mice way better”. And in 6 weeks, those that received medrysone, are way healthier than the ones that did not receive the molecule.
Now, if you talk about age. When a mouse is 24 weeks old he looks like a young human that is 40 years old. If you think about the time after remyelination, these 6 weeks can be something like 1 year for a human. So, if you have a drug that can make this 1 year be less painful, this is already something to be taken into account. If we replicate this to a human… Of course, this does not eliminate the necessity to look into humans, so that you mind what is this molecule actually doing. What we do know is, at least, in this more severe phase, which is those 3 to 4 weeks, medrysone is making these animals getting better.
What else is needed before we will have a medication for myelin repair? And how does the minimum time horizon look for that?
I think this is pretty close to happening because there are certain big pharmaceutical companies that are taking way more into account that precision medicine perspective in patients. Which is basically developing molecules that can be more specific to pathways and genes, that are disorganized in a whole bunch of patients. Because, back in time, when we were just looking into just one specific pathway, trying to regulate this specific one, we were really hopeful that this would work for everybody. And this is actually not the case. So, there are certain companies that are investing way more in precision medicine, which is basically investigating with more… quite robust way.
What we can call the genomic perspective, pharmacogenomic, which is evaluating which kind of genes this subtype of molecules can upregulate and this can be done in computers by bioinformatics evaluations and those technics just the genome sequencing in observation and the drug developing by informatics is already a cutting-edge technique to find new treatments. And this is something that most companies have been doing for 10 years, and to find a new molecule usually takes 17 years. So, maybe, in this range of 5 to 6 years… maybe even faster than this, because we could see during the pandemic how effective those companies can be to develop something that is beneficial, and they can work. I really believe that in 5 years from now we can have a groundbreaking molecule in the market that can treat certain types of MS, in terms of genome signature of patients. And make these people get better. I cannot tell you that I believe there will be a cure, but I believe there will be a molecule, or a bunch of molecules… because there are a lot of companies working together now.
For example, 2 of the biggest pharmaceutical companies in the world are now working together to produce an MS new drug. And this is really existing to be seen. It’s no longer a competition. There are companies, working together to make things go forward, so it’s a new avenue in the pharmaceutical companies, right now. Thinking way more about the patients than before and, improving these techniques of precision medicine is actually making them think about this. It’s needed to much effort to make things work and they are putting this together and making it so, hopefully 5 years for it to come.
Which breakthrough in research or treatment for people with MS would you like to see in the next 5 years?
That’s a good question. You know, there is one that I would like to see. I am passionate about astrocytes. I’m really interested about these molecules…. sorry, body cells. And I think, for me, it would be quite groundbreaking to show a molecule to specifically act in these cells. There is some already published, that are not using the clinic but you see they depend on the astrocytes to be metabolized, expressed into getting into the brain. I truly believe that using these cells, they are guarding our blood basically, because they have these end-feet that cover the blood vessels and make what we call hematoencephalic barrier, the called blood brain barrier. Kind of protecting the brain from other things we have in our blood.
And they are the ones that open the gate for these drugs that come through the blood stream into our brain. And we do know already that these cells are really special, for molecules to work inside our brains. There are really groundbreaking and interesting research correlating astrocytes and responses to the inflammation features and this kind of things. So, I think, there are pharmaceutical companies looking into astrocytes, to develop better drug delivering systems. Which is a molecule being more effective from going through the blood, into the brain. So, I think what would be really exciting for me is one drug that is addressed to astrocytes. I think this would be super interesting and groundbreaking in the literature. At least with the expertise that I have about these cells and all the ones that we have in the brain. Something more particularly addressed to astrocytes, I think will be quite successful as well. Not the response to all kinds of brain diseases in the world, but I think that astrocytes need to have more attention, as well.
How and where can interested people follow the most recent research activities?
In my LinkedIn I’m always sharing things that I found interesting about research. Sometimes, I do my own posts, otherwise I’m sharing what I think is interesting there. For me, if you’re interested in MS, for example, the MS UK portal is one of the key ones to be looking into, if you are a layperson or if you are an expert. You can get things regarding to that. As a scientist, my key portal to be looking into is basically PubMed, but if you want to know more about what I’m doing, my LinkedIn is actually the best recommendation that I can do to follow what I’ve been working with. For example, I’m planning to do a post next week, where I will address a little bit more what I’ve been working with some clients, regarding Alzheimer’s and also MS. I will not tell everything, of course, because of the patent issue and we are planning inside our company to start to share a little bit more of what we’ve been working, regarding health promotion, which is basically what we scientists are here to do. Even though we are in academia or not, we are here to promote health.
Is there anything else you would like to share with the listeners?
One thing in particular is that I love science communication, and I think this is really necessary to make science be better for everyone. And podcasts like the one that you have are actually giving people the opportunity to talk, is giving voice to express what they think about it. Every time that you listen, you will filter… you need to put something out of your mouth, out of your chest, do it kindly but always think about the audience. We, as scientists, we have changed the way that we talk about science over the years and I think that one of the things that makes me happy to be a scientist is how important science communication is today, so we can give people the right to know.
I think this is one of the most important things in science communication. It’s giving the people the right to know. Because we, as scientists, back in years we were thought we were crazy guys, with “Eureka” all the time, living in a dark place, not sharing, or not knowing how to explain what we do to people, and this was actually what media put out about what being a scientist was. And we’re not really like this. We’re normal people, who like to go out … I think one of the things that your podcast gives opportunities to scientists is to talk more in a simple way about their work, about their research. Science communication is for this, is for everyone.
Many thanks to Markley for the insight into the exciting research around astrocytes, their role in demyelination, and how to possibly stimulate them in the human brain using Medrysone.
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