It has been so enriching actually for me to be involved with the families. I'm all in. I do almost 99% of my time now is working on autism related stuff. I love this. It's a story of persistence and dogginess and not taking no for an answer, which anybody who does our business knows that's the only way through. That's the only way through. Absolutely persistent. Absolutely.
The human brain is the most complex structure in the known universe, and we are in the middle of a scientific revolution to understand its inner workings. Join us for a conversation with world renowned neuroscientists as they visit Rochester. I am Dr. John Foxe, director of the Del Monte Institute for Neuroscience at the University of Rochester, and you are listening to Neuroscience Perspectives. David Amaral, welcome to Rochester. Thanks so much for being here.
Yeah, I want to have a few minutes to chat with you about your thoughts about autism where we're at in the research field, where we're at in coming up with new ways to help treat these kids and deal with these kids, to transition these kids. So 20 years ago, people would say we'll cure autism in 20 years. We don't really say that anymore. Where are we at? Where are we at in delivering deliverables to these kiddos and their parents? Yeah, it's been an interesting transition.
20 years ago is about when I started in autism research. I started in it because five families came to our university, University of California Davis, and wanted to start the MIND Institute, which is Medical Investigation of Neurodevelopmental Disorders. And they wanted us to cure autism because they had children who were very profoundly affected by autism, sleep disorders and gastrointestinal problems, and they wanted those kinds of things to be cured.
And in the early years of my experience in autism, I sort of took their mantra and said, yes, what our mission was, was to cure autism. But I think we've wised up a lot and I think we've wised up in part because there are more and more people who are autistic themselves who have been able to educate us.
And I think where we're at now is that autism has a number of impairing conditions associated with it, whether it be anxiety that I'm very interested in trying to understand, or gastrointestinal problems, or sleep disabilities, or even something medical like epilepsy. And I think the field has come to the appreciation that those should be the targets for treatment. We should be trying to treat these impairing conditions.
While we obviously want to provide some social skills training and things like that to allow people to be incorporated into society, I think what we've learned is that we have to be more accepting of the condition. That people with autism historically have done enormously positive things throughout history. And the message should be that, you know, just like anybody else, we want to treat disabilities, but we don't necessarily want to eradicate the good features of autism.
So that's, I think, we've gotten a much more mature attitude on what our targets are for autism. I like that, mature. Exactly. Really, we've had a real maturation in thinking. There are two questions that come up every time I give a talk on autism, my own works, and related to autism as well. The first thing parents ask is, have we seen a massive increase in the incidence of autism? Or is it better diagnostic tools? Where are you on that? What's your thinking?
If there were a simple way to answer that question, you know, I could say yes or no, if there's been an increase or not been an increase. You know, what's happened is that it's, again, a much more complicated issue. So one thing is that our views of what autism is have changed over the last 50 years. So when Conor first described autism in the late 1940s, it was a seriously debilitating disorder that had certain features.
Our definition of what autism is has broadened. So we now consider more and more people. In fact, nowadays, it's not so uncommon for a 50 or 60 year old person to say, you know, I could never figure out why I was different throughout my entire life. Now I appreciate that I have a form of autism, but they weren't diagnosed at three years of age. They just realized that when they were 50 or 60. So I think one factor is that there really has been an increase in the spectrum.
We call it autism spectrum disorder, and the spectrum has broadened. So there's more individuals encompassed under that. I do think beyond that, that there are some biologically reasonable ways to think about, is there an increase in autism? So one of the examples I give is genetics. So we know that a certain portion of autism is caused by mutations of certain genes. Again, not simple because there's now more than 100 genes that we know are involved in risk for autism.
Many of these genetic mutations are what's called copy number variations. That means you have too much of the gene or you have too little of the gene. Well, it turns out that people have more and more copy number variations of their sperm and their eggs, the older they get. So we know that there's a very clear link between maternal and paternal age and whether you're going to have a child with autism.
And if you just look at the demographics of births in the United States, you know, 50 years ago, people were in their early 20s when they had their first child. Now they're in their 30s when they have their first child. So that's going to increase the number of people with autism simply because of that genetic characteristic. We don't know how much that contributes to it. People have talked about various other kinds of environmental factors.
Maternal infection, we in California worry about exposure to pesticides. And at our institute, we have people who have shown that, again, if you have an exposure to certain kinds of pesticides or other environmental toxicants, it can slightly increase your risk of having autism. So to answer your question, finally, I think probably the number of people with autism has increased. And it's due to a number of factors. And we really don't understand how those factors all come together.
And because of all these things that I've mentioned, we don't really know what the numbers were 50 years ago and what they are now. But the bottom line, I think, is that when you have one in 60 children in the United States diagnosed with autism, that's an enormous number.
And we need to understand what are the causes. And of course, what we're all trying to do is do earlier diagnosis so that we can get kids into earlier treatment so that their quality of life is as good as possible for the rest of their lives. To what extent, then, is better diagnosis and more awareness in the clinical communities playing a role as well? And the fact that we now know that one in 60 children is born with autism, that's a big thing.
I agree. Even though if you're at a place where you have a well-trained clinician, psychologist, psychiatrist, who knows about autism, they can make a pretty clear diagnosis by 18 months, maybe as old as 24 months. The reality is that in the United States, the diagnosis happens beyond four years of age. So it's getting better, but what we do need is more highly trained clinicians. And there's a number of strategies.
There's something called the Eco Autism Program, where places like the MIND Institute are actually reaching out to rural practitioners in order to educate them about autism so that they can make those earlier diagnoses. So I do think that it's gotten a lot, lot better than it was 50 years ago. It can still get much better. Now, the other thing, of course, is we don't have it yet, but it'd be wonderful if we had a biological marker or markers.
I don't think that there's going to be one biological marker that's going to detect autism. But if we could, like phenylketonuria, where you take a little drop of blood when the baby's just a newborn and say, OK, this child has this disorder, PKU is actually my poster child for autism.
I don't know if it'll happen, but I'd love to have something like this, where when you can detect PKU in a child that's a newborn, simply by changing their diet, you can change the life course of that child from having profound intellectual disability to having a near normal existence for the rest of their lives.
So we don't know yet whether by having a blood test or some other biological marker early in life in autism, we could intervene enough so that we could change the life course of that child. That's one of my hopes and one of my goals. It's a chicken and egg situation. Until you have that measure to do the very early detection, you can't test whether you have ways to change the course. That's right.
And getting after that, you really answered my next question, which is where are we at with developing markers? Brain imaging, of course, is a big one for you personally, but brain imaging, electrophysiological markers for the early detection of autism. Right now, it's mostly done with neuropsychological evaluations in youngsters by clinicians. That's right. Are we getting close at all? I think we are.
There's a lot of tantalizing hints in the research arena that one or more kinds of efforts will produce biological markers. So as you said, now you have to do a behavioral test. Even the best clinicians aren't willing to really make a call until about 18 months. They can tell that maybe there's some danger signs, but they're not saying, willing to say this is autism. In some cases, I think the genomics and metabolomics, we did a study looking at blood samples from young children.
And you end up with thousands and thousands of metabolites. So these are small molecules that are in the blood of the child. And we asked, are there any signatures that are different in the children from typically developing children? And I guess the bottom line of that study so far is that there was no one signature that could differentiate all the kids with autism from the kids who were typically developing.
But what we did find was that, and I won't go into the details, but one change in amino acids could actually predict at high reliability 17% of kids with autism. We're working on other changes in metabolites where we now think we can, by adding them together, we can probably detect something like 30% of children with autism. So again, I think what we've all realized is that there's not going to be one cause of autism. There's many. And there's probably not going to be one biomarker.
There are going to be many. One of my former graduate students, Mark Shen, who's now at the University of North Carolina, has continued to pursue an imaging strategy. We found years ago, almost by accident, that young children that are the brothers or sisters of children with autism, so they have a much higher likelihood of having autism, they had what we called increased extra axial fluid.
And that means that if you take an MRI of their brains, the fluid in between their brains and their skull was enlarged. They had more of this fluid. And so Mark, as part of his thesis, actually measured the amount of extra axial fluid. And it turns out the amount of that extra axial fluid at six months of life is a pretty good predictor of whether a child is going to go on to have autism or not.
And we've now confirmed that in children that are three years old, they continue to have that increased extra axial fluid. So I do think we're getting close. Speak to that, though, because people will want to know, well, why is it important to know at six months? What doors does that open for us? Right. So where you go from there when you have a diagnosis, you can get children into early interventions, as early as 12 months. And it has an enormously beneficial effect on those children.
So again, the reason we're trying to do everything earlier is that you have this window of opportunity. When a child is born, their brain is about 25% of the size of what it will be when they're adult. By the time they're six, it's 95% of the size. And the notion is that something happened prenatally that has changed the way the brain is organized. But the brain can adapt, particularly if you have the right interventions.
So by getting the child into intervention at 12 months rather than, say, at four years or five years or six years, it's much more likely, and there are data on this now, that the earlier you get children into intervention, the more likely you are to show a positive benefit to that child. Another thing that I've matured on is that when I used to write papers about autism, I would say autism is a lifelong disorder. It turns out not necessarily to be the case.
So many children who are, in fact, in our own studies, we've shown that many children who are diagnosed at two or three with autism, by the time they're six, have lost the features that would lead to a diagnosis. We have a colleague at the University of Connecticut, her name is Dr. Deborah Fine. She's coined the term optimal outcome. But to me, what it means is that there's enormous potential for plasticity in the brain at their early ages.
And if you can intervene and allow a child who would have had, again, a very serious form of autism, to have a form of autism that can be managed through other processes, that child may go on to college and have a family and just have a normal life. So that's why we want to get in early and intensively. And I think that's a really key message, because of course, for a parent of a six month old, having their child labeled with a diagnosis like autism is a painful and difficult time.
But the point is that this gives clinicians and researchers a huge window to make to change the course of a life. Very well said. Now, I would be remiss, and I know everybody who works in the autism field hates this question because we're tired of answering it. But I would be remiss if I didn't ask you to give us 20 or 30 seconds on vaccines. We're sitting in the middle of another measles crisis of all things in the US at the moment. So tell us where you're at with that.
Well, I really hardened on this. I think, first of all, there is absolutely no evidence whatsoever that vaccines cause autism, particularly the measles, mumps and rubella vaccine that we're here most about. The notion that it causes autism came from a flawed and now retracted paper. And unfortunately, humans tend to be superstitious. So when they hear something concrete, they tend to buy into it. And it's hard to change people's minds.
And on the other hand, I think people are looking for an answer. You know, scientists at this point are still struggling to say, you know, what caused your child's autism? And we can't give a straightforward answer. But I've really looked at the data on whether the MMR vaccine can cause autism.
And, you know, there have been papers and papers and papers showing that both in the United States and other countries, if you look at all of the epidemiological data, there was a meta-analysis that was done just last year based on 15 million children. Fifteen million. Now, if there was any signal whatsoever, if there was any indication, even a minimal risk, that the MMR vaccine would cause autism, you would have seen it in that analysis. But there just wasn't.
And so the tragedy is that measles is a devastating illness to some children. When I was in San Diego, we had a neighbor whose child contracted measles and then ended up with measles encephalitis and died when they were six. This is a preventable disease. And I think with more and more children having measles, there's going to be more death, there's going to be more disability, and it's entirely preventable.
And I'll tell you, one of the things that convinced me in my own research that, you know, probably we shouldn't be even worrying about the MMR vaccine is that I've become convinced that everything that probably leads to autism happens prenatally. Long before the child has the vaccines. The reason that a lot of parents think that the vaccines might be related to autism is that you have the MMR vaccines at 12 months and 24 months. Right.
And so there are two, I'm going to simplify, but there's basically two forms of autism, how it starts. In one form, the child, even when they're really young, like 12 months, you know something's wrong. Right. And they're not making eye contact. They're really, you know, this is based on really good research that looked at first birthday videotapes and quantified how much time the child is enjoying the party, making contact. And so we call that early onset autism.
But then there's another group of kids, and it's about 50-50. Again, I'm oversimplifying, but it's about 50-50. Right. That at 12 months of life, you look at them, they're smiling, they're enjoying things, they're learning, beginning to learn words. For all practical purposes, they look, you know, essentially typical in terms of their development. And then something happens between 18 and 24 months and they regress into autism. Right.
And so occasionally a child will have the MMR vaccine and then that regression will take place. And there's an association then between the vaccine and the onset of the autism. But it's correlation, it's not causation. And so we did a study where we tracked young kids essentially from birth and we were following them now, they're in middle childhood. And we were able to look at their head circumference sizes, which is a proxy to their brain size.
What we know and our research shows is that there's a subset of children that have increased head circumference and then increased brain size. And so we looked at whether we could detect that, when we could detect that in kids who had regressive form of autism. It turns out that the brains of the children were starting to change at four to six months after birth, okay, long before they even had the first MMR vaccine. But they had regressive form of autism.
So this is another thing we've learned is that a lot of neurodevelopmental disorders happen early on, but there's no signs and symptoms of it until much later on. Even nowadays, my colleagues who study schizophrenia call schizophrenia a neurodevelopmental disorder because they think it's something that happened prenatally or really early on. But you don't see the schizophrenia until 20 or 30 years later. Right.
So again, the bottom line is that I don't think, you know, the MMR vaccine has anything to do with the onset of autism. And I think if parents don't become aware and public policy doesn't become more aware that it's just not okay to not vaccinate your children because you're not only affecting your child, you're affecting everybody else in the community.
And I think we have to have some social awareness and social consciousness that this is important not only for our family, but the larger family of people. Right. I grew up in Ireland and the MMR vaccine hadn't reached the countryside. So in my own family, I have a profoundly deaf cousin as a result of rubella, measles and so on. Yeah. So I mean, we and you see the devastation that something as simple as measles can wreak.
Everywhere you look at it, I think, you know, vaccines are one of the, I think, wonders of medical science. Yeah. And I do think, you know, there's something and I don't quite understand this. I think sociologists and others need to be able to explain this better. There is a certain reluctance on the part of the public to believe medical science and believe people like us, you know. And I think we have to do better to educate people, you know, and inspire confidence in them.
It's, you know, we've long gone past Marcus Welby and, you know, some of these American doctors who were so well-off. I think, you know, as a field, we have a communication problem. And maybe, you know, maybe it's an old trope, but, you know, scientists, we're busy in the lab, we're maybe not the most social people in the world. So that's why I'm glad you're here on camera with us today. You couldn't have possibly said that any clearer. Thanks for doing that.
OK. Thanks. Let's stay with controversy. OK. OK. We're not going to let you off the hook there. Yeah. Speak to the people who are watching in about the key importance of animal models in research, particularly around autism. I think, on the one hand, the best model for studying autism is people with autism, autistic people.
But when we're trying to get to the point of understanding the mechanisms for what's causing autism, it's really hard and, of course, unethical to try and do the studies that need to be done in human subjects. So I'll give you an example. I mentioned that some of our research points to the fact that a subset of children with autism have big brains. And it turns out that it's 15 percent of boys who have autism have really enlarged brains. We call it megalencephaly.
In our study, we found that these kids tend to have even more intervention because they're doing so poorly than the kids who are doing better, but they just don't respond. And so the question is, why? Maybe if we understood why their brains are enlarged or what's going on in their brains, we could maybe have an answer to a medical intervention or something else that could be helping. Well, we don't understand why their brains are larger.
We don't understand whether they have too many neurons, whether they have too many connections. And I do a lot of MRI, and we've really probed these kids with our MRI. But MRI can only get you down to a certain level. It's like looking at the earth from 30,000 feet. You can't see an individual tree or you can't see a rose on a bush. And we really need to be able to understand these kids at a cellular level.
So we and others are trying to create animal models of this phenomenon so that we can understand the basic molecular mechanisms, neurobiological mechanisms. So hopefully that will give us a hint as to a more effective treatment. I think it's perfectly ethical to try and understand a human disease by, you know, you mainly ethically and, you know, do studies in animal models. I'm a strong proponent of only doing what makes sense and not, you know, certainly not do wasteful animal research.
You know, things like testing drugs. You don't want to test drugs on people. You want to test drugs on, you know, on either animal models or another bioassay. And, you know, having said that, while I feel it's perfectly appropriate, I do think that science is moving forward with some really intriguing new strategies that is going to reduce the number of animals.
So when I was a graduate student here, the idea that I could take a few of your skin cells and turn them into your neurons, which was completely science fiction. Right. We're doing that now at the MIND Institute where we bring in the children, particularly these children with the big brains. We take actually we don't even have to take their skin cells.
We just take a little blood sample and then our colleagues are transforming them into what are called induced pluripotent stem cells and then transforming those into neurons and glial cells and all the parts of the brain. And we're able to understand, you know, what may or may not be different in the regulatory processes in those neurons.
And then like other forms of science, we could take potential drugs of treatment, squirt them on the neurons in a dish to see if they normalize whatever's wrong with those neurons before we squirt them into the child. Right. I think as long as we need animal models, it's perfectly appropriate. I do hope that we will continue to get more advanced other assays that will reduce the amount of animal usage to, you know, what is absolutely essential. Yeah, of course. Policy. Let's turn to policy.
In the morning, we're going to assign you as the NIH czar for autism research. What would you do to shake up the field? Are we doing it? Are we doing it the right way right now? Is it all working as best it can be? Or are there things that we could do as a field, as a community that would really, you know, break the back of this thing? Yeah, that's a really good question. It's, again, a really hard one to answer. So I sit on a committee called the Interagency Autism Coordinating Committee.
What is clear is that autism still is in, you know, sort of deficit of in terms of the resources that are needed to do what needs to be done. So we recommended last year that the amount of money that goes into autism research annually now is about three hundred and fifty million dollars. The IACC recommended that it be doubled.
Now, so the first thing I would do is I would try and put more money into autism research because I think it's not the case that it were saturated with good science, that there is a lot of good science that's not getting done. Exactly. That we don't have the funding. And, you know, the other thing is that I think not all autism research can be done in a standard five year grant cycle. So one of the things that we've done is we were trying to do a longitudinal analysis of children with autism.
And, you know, we've been fortunate that we've gotten different kinds of NIH funding and now we have an autism center of excellence that's funding that. But it really was a lot of work to try and hobble together all of the funding necessary to we have now over five hundred families that are involved in this project.
And, you know, it would be so much nicer if there would have been a project, maybe even a multi-site project, that would have said, OK, we want to understand the life history of autism. So we're going to start with families that are thinking about having a child, take blood samples from the mom, from the dad, understand the genetics, do sampling through prenatal life.
So we understand whether there were any medical problems with the pregnancy and then start analyzing maybe annually the child as they grow up to really try and number one, parse autism into more homogeneous subtypes, but really to understand, you know, what are the causes, you know, prenatally that affect things postnatally. There's no study in the United States going on like that. There are environmental studies that are pretty big.
There's genetic studies that are pretty big, but there's no environmental studies that are hooked to genetic studies. And neither of those are hooked to imaging studies. So I'll tell you one other thing. We were talking about animal models before. And I am so I think that for some of the studies that we're going to want to do in the future, to most of the research is being done on mice. And that makes sense. Mice are a reasonable proxy for certain aspects of our biology.
But for certain other things, the non-human primate is going to be the only reasonable proxy for particularly for interest in understanding social impairments and cognitive impairments. I think we're going to have to do at least some work on the non-human primate and particularly to understand how the genes that have been linked to autism, you know, produce autism and what are the brain changes that those genes bring about.
Our colleagues in Japan and China have realized that this is probably going to be the future of biomedical research and have invested heavily in transgenic models in the non-human primate for probably for the last 10 years. And they are actually leading us by far on this area.
The NIH has been slower to embrace the notion that we can do genetic models, even though you hear in the news nowadays that people are worried about whether there's going to be genetic models, you know, using this so-called CRISPR-Cas technique, which is actually a pretty straightforward and exciting technique. They're actually taking gene editing to do gene editing. Yeah. People are worried about whether they're going to gene edit people.
Right. You know, and which I agree, I don't, you know, I think we need to put the brakes on that right now. But that technique could actually be used in non-human primates to create, I think, you know, again, in a reasonable and ethical way, some very useful non-human primate models of autism. It's happening in other countries. It's not happening in the United States. So again, if I could wake up and change something at the NIH, so to say, let's get on with that as well.
When you were nine or ten years old yourself, did you know you were going to be a neuroscientist? Did you ever think you'd be in this position? Was that the dream? You know, I was always pretty much a nerd, not a neuroscientist. I was always interested in the issue of social behavior in my late high school years and early college years.
I was really a big fan of B.F. Skinner, you know, psychologist who developed a lot of the behavioral strategies that ultimately were used in some of the intervention techniques in autism. I once wrote to B.F. Skinner. I got a note back, which was really one of the highlights of my teen years. In the frame on your wall? Yeah, I have it at home. I have it at home. I haven't lost. He wrote a book called Walden II, where basically through use of operant conditioning techniques, it was a utopia.
Everybody got along. Of course, it sort of did fall apart. There were some models that tried to do that and were more complicated than just what learning techniques can try and control. But I guess I was always thinking that I would go into some form of biology at some point in time and really got interested in it when I went to Northwestern as an undergraduate. Had a terrific faculty, a psychology faculty member whose name is Arya Rutenberg, who's unfortunately passed recently.
And he taught the introduction to brain and behavior. And went to that course. And it just like, oh, so there was always something missing about B.F. Skinner because Skinner was only the psychology. But I always wondered, what is it that's causing this? And Skinner, for him, the brain was a black box. He didn't care about it. But clearly, that was where all the really cool stuff was happening.
And if you could only understand the brain, you'd really be able to modify behavior and hopefully help people. And so when I went to this course by Dr. Rutenberg, it was like, oh, this is really it. This is my playground. This is my playground. And I almost immediately, I went to, this is my sophomore year in Northwestern, and I went to Arya and said I wanted to work in his laboratory. And he said no. My parents are paying for me to go to Northwestern. I want to work in your laboratory.
And he said no. So at the time, I was sort of persistent. And I went back to him again. And I'd love to, I'll volunteer to work in your laboratory. And he said no. And I went back a third time. And so I can remember, we were sitting in a microscopy room together. And he said, OK, you took my course. Tell me how the cerebellum works. Well, you know, I don't really know. I knew the platitudes about the cerebellum. And fortunately, I said, I really don't know.
And he said, OK, as long as you're going to BS me and tell me some myth about the cerebellum, I'm going to let you work with me. And that was, it was like, you know, he passed a litmus test. And he wanted to know whether I was going to be persistent enough. That was the beginning of my career. And I went from there to here, University of Rochester as a graduate student. And haven't looked back.
I think in my early career, the first 20 years or so, I was doing really basic science, trying to understand the circuitry of the brain and the function of the brain. I was very interested in memory and in emotion and social behavior. I worked on parts of the brain that we thought we think are involved in that. And really wasn't all that interested in clinical research per se until the parents who wanted to start the Mind Institute came to us.
And, you know, I just was so empathetic with the really difficult life they have. I mean, it's what a lot of people don't understand is that many children with autism, you know, they have a sleep problem. What's the sleep problem? They don't. They don't sleep. So, you know, three of the families that started out of the five that started the Mind Institute, their children would sleep about an hour and a half a night.
So, you know, imagine what this that does to a family life, to marriage life, you know, and their kids would just take off. They, you know, they would try and leave the house. And so they always had to be monitoring the children, you know, all the time. Their kids had GI problems, so, you know, they could just not have a normal family meal.
And, you know, so it seemed to me that, you know, this is something that, you know, potentially could impact the family and the child for the remainder of their lives. It's relentless. It's relentless. The task in front of parents and siblings and the child itself. Absolutely. Absolutely. So finally, I, you know, it tickled my empathy. And you relented. And I relented. And I, it has been so enriching, actually, for me to be involved with the families. I'm all in.
I, you know, I do almost ninety nine percent of my time that was working on autism related stuff. I love this. It's a story of persistence and doggoness and not taking no for an answer. Which anybody who does our business knows that's that's the only way through. That's the only way through. Absolutely persistent. Absolutely. Last question. Okay. When you're not when you don't have your science hat on you, you're a self-admitted nerd. Yeah. What do you do? What's what what floats your boat?
I'll say three three things. I love spending time with my wife and we have a golden retriever dog and so taking walks with them, you know, that that's just sort of the part of the relaxation. One of the things that I'm just getting back into is music. When I went to when I went to Northwestern for a while, they was toying with the idea of either going into music or going into science.
And I fortunately met a lot of the musicians because I was taking the music courses and they were so much superior to me in every respect in terms of music and decided it's probably easier to be to go into science. So I did I did that. But I taught guitar and played guitar when I was at Northwestern and and and subsequently, I sort of got away from it, but I just just actually this year bought myself a brand new guitar, which I love and I've been playing some more of that.
Amazing how many people in the sciences are musicians as well that it gives them that creative output because there's it can be a slog in science. And so to get home and to work on a piece of music. Yeah. Yeah. Creativity as well. It's absolutely true. Crosses the two disciplines. So music is one thing. And I guess the the last thing that is I like the ocean. I was born in Massachusetts and we have a little house out in Cape Cod.
It might be sound crazy that we live in California, but we go to Cape Cod for the summer. But it's like sort of like a lemming going to the sea. You know, I imprinted on the even the stinky smells of the ocean, you know, just and I we my wife and I and the dog often spend time on the on the East Coast.
And, you know, the antithesis to to the academia or the science where you're constantly thinking, constantly worrying about your next grand and things like that is that I go out and I go clamming, which means I take a rake. I go in about a foot of water and I like a farmer go out there looking for co-hogs. And, you know, and the nice thing is that you get better at it over time. And so I get enough. So I'm just getting peace.
And this yet so you get out there, you know, six thirty in the morning and the seagulls are flying over and it's a sunny day and the boats are going out. And, you know, it's just completely peaceful. So when when you know, I'm worrying about a grant, sometimes I'm thinking about doing that co-hogging. But I am very passionate about the science that we do. We have a tremendous team of people.
That's, you know, all of the stuff that I've talked about that I say we do at the Mind Institute really is based on a group of people that are contributing in different ways. And it's very exciting time. I'm very optimistic. I know that families who have children with autism are, you know, constantly saying, you know, how come we don't have an answer? And I think, you know, it's because the question is so difficult. I mean, autism is really complicated, difficult to understand disorder.
But we are making we are improving. We are, you know, making progress. And I do think that, you know, as we focus more and more, as we talked about at the very beginning on trying to treat things like anxiety and epilepsy and GI, you know, we may not solve the entire problem. And again, as we talked about in the very beginning, maybe that's not shouldn't be the goal.
Maybe, you know, to have an autistic person who, you know, is not no longer anxious or no longer has the threat of an epilepsy, that that's fine. Then we declare victory and move on. I often say that to parents. We would love to throw a 90 yard touchdown. Yes, we're doing it inches a foot a yard at a time. But we are making progress. We are. We are. David Amaral, thanks for being here. The Del Monte Institute. Welcome home to the University of Rochester. I enjoyed it. Thanks very much.