First Annual Three Minute Thesis Competition

[Speaker: Scott Weber] Our next presenter is Mohammed Atif Afzal, and his title is "Accelerated Discovery of High-Performance Materials." His major advisor is Johannes Hachmann in the Department of Chemical and Biological Engineering. He loves tennis, puns, and not to be outdone also speaks four languages. So ready, set, pitch.

[Speaker: Mohammad Atif Afzal] Let's consider a scenario, let's take two cups. One made out of a plastic material, and another made out of a glass material, and drop them both on a hard floor. What happens? Of course, the glass material breaks and the plastic material remains intact. You're probably imagining what if your phone is made up of complete plastic materials. You will never have to see something like that. Well, the problem is the current existing plastic materials do not have sufficient properties to be used in such devices. In my research, I am designing new plastic materials so that the phones never break.

One interesting thing about plastics is that the molecules that can make plastic materials is basically infinite. That means there exists a combination of atoms that can make a plastic material with a targeted property. However, it's a challenge to find right combination of atoms in this huge molecular space. Therefore, in my research, I'm designing millions of potential molecules and then computationally evaluating them using an infrastructure which is built using complex calculations and all the calculations are performed on a supercomputer. Now we have calc values of millions of molecules and we have large amounts of data. We can look at the data and understand what's going on with the molecules and how the molecules are behaving but a human brain can only look at few molecules and maybe design a new material based on intuition, which is what scientists have been doing in the past.

But, finding patterns in millions of data is quite not feasible. Let's consider a classic example of needle in a haystack. It's nearly impossible to find the needle with our bare hands. But we can accelerate the process of finding the needle by creating robots and teaching them to find the needle for us. In my research, I am using a very similar idea. I am creating an automated framework. That can basically find the atoms of combination of atoms so that we can design the material with the targeted property. I am doing this by basically teaching the computers to learn from the available data which is called machine learning. And the particular algorithm that I use is called neural networks. This is because it works very similar to how our brains are operating. Let me tell you that this technique is being used bi-tech giants such as Google, Microsoft, and Facebook, to do tasks such as facial recognition and voice recognition.

In my PhD thesis, I'm extending these techniques so that I can discover next generation of high-performance materials so that our phones don't break and because I’m using plastic materials our phone can be flexible lightweight and also cost-effective thank you.

[Applause]

[Speaker: Scott Weber] Thank You Muhammad.

[Speaker: Scott Weber] Our next presenter is Peter Bloomingdale. Peter's title is "Networks, Nerves and Cures." His major advisor is Donald Major in the Department of Pharmaceutical Sciences. Apparently, he cooks great Indian food and is a challenge shoe shopper, and has not been into Harry Potter … I don't know where that's going but we're going to let him play that out so… Ready, set, pitch.

[Speaker: Peter Bloomingdale] When I began my PhD, I always envisioned curing a disease. Initially I want to cure cancer, high hopes I know. But after reading about cancer, the different treatment options that are available, I became interested in the adverse effects of chemotherapy. My research focuses on one of these: chemotherapy-induced peripheral neuropathy.

Chemotherapy is the use of toxic chemicals to kill cancer. However, this is essentially a poison. When this poison enters our body, it distributes everywhere and damages everything in its path. When it distributes to our peripheral nervous system, it causes nerve damage known as peripheral neuropathy. Patients that develop peripheral neuropathy will feel a numbness and tingling sensation in their hands, feet, that travels across their body. Now, the problem is, is that this will turn into an extreme pain. The goal of my research is to prevent this pain, to prevent peripheral neuropathy from occurring. And to do so I built a biological network of our nerve cells.

To give you an analogy, I'll use a network that we're all familiar with Facebook, the largest social network. Here dots represent people, connections between these dots are people, are friends. It's very similar in a biological network, except for the dots are genes and proteins inside the cell and the connections between these dots are how these genes and proteins interact with each other. Now if we take everyone who's on Facebook and look at their physical location in the world what would we see? We would see something that looks exactly like this. Pretty amazing, right? Upon zooming in you would notice that people are clustered together in cities. In a network theory, these clusters are termed “motifs.” Now motifs are important and very interesting because they relate to function. Now, if you looked at New York City you'd see people clustered around there that form a motif. Its functions related to the economy, it's the economic powerhouse in the United States. Whereas in biology genes and proteins cluster together to form these motifs, such as the mitochondria which relates to energy production, the energy powerhouse of the cell.

So, for my research, what I've done is I've analyzed the motifs in this network of our nerve cells. I then looked at healthy nerve cells compared to nerve cells that have been damaged by chemotherapy and interestingly, I identified two motifs that become damaged. One is our mitochondria and the other involves our immune system. This network based approach has allowed me to identify a novel drug to prevent nerve damage and pain associated with chemotherapy, potentially curing peripheral neuropathy. I'm currently testing this treatment in mice and hopefully one day I'll be able to try this in humans.

[Applause]

[Speaker: Scott Weber] Thank you Peter.

[Speaker: Scott Weber] Our next presenter is Antonella di Giulio whose title is “Fountain of Youth for Brains, a Map of Sounds.” Her faculty advisor is Brian Mosley and she's from the Department of Music. And she was born in Germany, but clearly Italian, and speaks four languages and sort of super great to have her here. So, ready, set, pitch.

[Speaker: Antonella Di Giulio] Would you like to live forever if you think probably not but would you like to be forever young, maybe yes? We haven't found a fountain of youth for our bodies, but we might have found one for our brain.

Our brain is a powerful instrument. Its 90 billion nerve cells and an infinite number of pathways for the brain signals to transmission. The bad thing about the brain, is that it will start to shrink at a certain point in our life. But here's the good news. We have a powerful anti-aging product, which is music. Researchers have shown that just listening to music can improve our cognitive abilities.

However, many researchers when dealing with music they feel lost because they lack knowledge in music theory. They cannot really identify which combination of sounds is influencing the brain and why? So what if this researchers could use a kind of a GPS to navigate complex music analysis. They will be able to translate sound information that music theories will give them into the data for their research. That would be awesome right?

So let's compare the different musical genres to places on a map, and then let's compare a piece of music to a route from a starting point to a destination. The central point of orientation on this map are particular elements of sounds, main characteristics of the route or special effects. In a three-step process, my sketching method is translating traditional music analysis into an easy-to-read, but detailed 3D map of any piece of music. The first step, we look at another view of the piece and will identify the main point of interest. The second step will aim to identify the details of the point of interest and then discover similarities and differences. The third step will summarize the information into one single image. To this, the system researchers will be able to use this data as a GPS. They will be able to find the fountain of youth and then they will help keep our brains young. And so, keep in mind that music is a fountain of youth, thank you.

[Applause]

[Speaker: Scott Weber] Thank you, Antonella.

[Speaker: Scott Weber] Our next presenter is Lucie Kafkova, whose title of her dissertation is “Figuring out African Trypanosomes, Protein at a Time.” Her faculty advisor is Lori Reed in the Department of Microbiology and Immunology and some things that she'd like us to know is she owns a sugar glider and quite frankly I had no idea what a sugar glider was until I looked it up, and I'm not going to tell you unless you, you may already know. She loves magic, dragons and heroes. So ready, set, pitch!

[Speaker: Lucie Kafkova] In a world where everybody asks where is the prophet? Basic science works with slightly different equation, you put the money in and what comes out is knowledge. Basic science is driven by human curiosity, and I am very curious about molecular biology of African Trypanosomes.

Trypanosomes are single cell parasites that live in human blood and cause the sleeping sickness. Don't worry, you do not have it unless you went to Africa, got bitten by a really big ugly fly and now you are often feeling like you have a bad flu. In that case, you should get yourself checked. The disease is deadly and not treatable when caught too late.

I know molecular biology can sound intimidating. So, let's make it more fun. Let’s imagine the trypanosome as a Rube Goldberg machine. The receptor on the surface picks up an input, sends a signal into the cell, the signal then travels through a protein cascade until ultimately causing a certain outcome that will be helpful to further trypanosome to deal with whatever the input meant. Except it is not quite this simple. Trypanosomes contained over 10,000 unique proteins that participate in thousands of very intertwined pathways like this one.

My task is to find out as much as I can about the protein that modifies the shape and therefore function of hundreds of other proteins. So how do we do that? Well my favorite way to start is to create a trypanosome that cannot make that protein and then look for what breaks. Did it stop moving? Is the metabolism broken? Can it divide? Then we can also lyse the cell causing the whole machinery to spill out, isolate our protein of interest and look for what sticks to it. Once we think we know what's going on, we can make the proteins, put them in a test tube and try to replicate simple events that take place in the cell.

By these and other methods, I have discovered that my protein of interest, actually, in order to do what it's supposed to do, has to be in a complex with very similar but slightly broken protein. This was very surprising because in humans and other organisms this class of proteins tends to work as a unit of two identical units. So, I'm very curious about how this novel arrangement is going to prove advantageous to the trypanosomes or what's going to happen next.

Anyway, why am I doing this? Is it really worth spending several years of my life to find this function of a single protein in an odd parasite? I think so. We are uncovering the secrets of life, one puzzle piece at a time and often the pieces that go together come from very unexpected sources. We never know what's going to prove very crucial in the end and therefore we need to keep trying to find out everything we can. Thank you.

[Applause]

[Speaker: Scott Weber] Thank you Lucy.

[Speaker: Scott Weber] Our next presentation is from Holly Keily whose title is “Gesturing to Make a Point: Who is that gesture for?” Her advisor is Jürgen Bohn— I'm sorry Bohnemeyer, from the Department of Linguistics, and you know Holly's got some pretty interesting things going on. She has been all over the world, she's a soccer certified referee, loves, snow enthusiast and she's an expert in pearl. Ready, set, pitch!

[Speaker: Holly Keily] We wave our hands around when we talk. It's okay, everyone does it. It's fine, we're gesturing. We use gesture to help us describe the size or shape of things, like: this fish I caught that was actually, it was this big, you'd never believe that! We use gestures to give people directions on how to get places, to explain how things work, like a Rube Goldberg machine. We use gesture when it doesn't seem to mean anything at all. So, what is the point of doing it? You can understand me without seeing my gestures, and I can talk to you without gesturing, but that's not what people do. We use gesture.

Who are we gesturing for? There are two kind of answers to this. I could be gesturing for myself, the speaker. I can be gesturing to help me remember what I'm going to say or think of the word that I want to use. I could be gesturing for you, the audience. I could be trying to direct your attention to me, or something else, or I could be gesturing to illustrate something for you so that you can come up with a mental image of it. I want to know which one we're doing.

I had people watch events and then describe them, and I watch them describe things to other people. I found that we have a negative correlation between the rate of gesture and the length of a description, so that means that I get really short descriptions with a high rate of gesture; a lot of gestures. I'll get something like the following: there's a girl and she has this kind of like mallet thing [waves hand in a circle] and a long stick in front of her and she takes the mallet and she smashes the stick [swings arm to represent hammering motion] and it goes everywhere. That’s like 25 words and maybe eight gestures, that's a lot.

I also get really long descriptions with very few gestures. So, I'll get something like this. There’s a girl and there's a table and there's a stick on the table and the tables may be trapezoidal I think it's kind of a light brown color but it looks like it might have a tablecloth over it, but anyway, she has a hammer and she uses the hammer to smash a stick [hammering motion] and it goes all over the place and some of the pieces land on the table and some of the pieces land on the floor. That's like 50 words and one gesture. That's a little unusual, that's unexpected, it's not what I thought I would get.

What does it tell us? Well it kind of tells us that we are gesturing for the audience, because if I was gesturing to help myself as a speaker I would expect that as I say more things, I need more help and so I gesture more to help myself more so I can say more. That's not what people get. That's not what we're doing because implies that my gestures are something that I'm doing to try and communicate to you specifically. I want to visually highlight, underline, bold, italicize, or emphasize something that I think that you should think is important. So, who am I gesturing for? Well, at least when I'm describing events I'm gesturing for you. Thank you.

[Applause]

[Speaker: Scott Weber] Our next presenter is going to be Gokhan Kul, and his title is "Et tu, Brute?: Detecting Insider Attacks to Databases.” His major faculty advisors are Shambhu Upadhyaya and Oliver Kennedy and they're in the Department of Computer Science and Engineering and I don't know if he's in, I don't, he likes to play guitar, he was going to be a scientist from an early age, but when he took a little break, he watched a little Gossip Girl apparently. So, Ready, set, pitch!

[Speaker: Gokhan Kul] Friends, Romans, countrymen, lend me your ears, and imagine a world where Julius Caesar had not gotten stabbed by his friend Brutus. In that world, maybe he would have conquered Britain, maybe William Shakespeare wouldn't have written his play “Julius Caesar” and maybe his name would be Marco Shakespeare instead of William. Enough counterfactuals though, let's fast-forward to our century.

I'm sure you have heard the names Bradley Manning and Edward Snowden on the news. Although they were trusted people, they stole critical intelligence documents and released them. The worst came later in 2015, the Office of Personal Management of the U.S. disclosed that someone had acquired personal information of 22 million federal employees, including employees with the highest level of security clearance. Whoever the thief, they put the security of the entire nation at risk. They risked your families, they risked your friends, they risked your freedom. Did they get caught by the security measures in place? No. Remember, there are layers and layers of security measures in these systems, against hackers, but an employee, is already inside these layers and may have access to a lot of information that nobody had.

My research focuses on detecting insider attacks to databases, attacks coming from people you trust. I monitor behaviors of users and how they interact with organizations database. I use the query logs and these query logs are the records of questions that people ask to the database and the way they ask them.

We collected three real-world data sets, one from a national bank, one from smartphone applications, and one from student assignments to understand how people write the queries. We use these queries to create personal profiles. The detection mechanism depends on these personal profiles and uses statistical Information, statistical methods to understand what the change is about.

You may think that maybe we are overreacting, we should trust our employees. That is correct. Completely correct, but better be prepared, better be prepared than sorry, right? If you don't believe me you may ask my friend Julius Caesar over there, I'm sure he will watch for me. Thank you.

[Applause]

[Speaker: Scott Weber] Our next presenter is Kristin Maki and her title is "Is a Story Worth a 1,000 Numbers?" Her major advisor is Thomas Feely in the Department of Communications. She's a map carrier, apparently, a hockey player and has a memorized chocolate chip recipe, if you need it at the end of the presentation. Ready, set, pitch.

[Speaker: Kristin Maki] In 1985 Lisa had to have a blood transfusion. She was worried because this was before transfusions were routinely screened for safety and HIV was on everybody's mind. But she felt OK afterward and she's been pretty healthy since then, aside from feeling tired at times. But the last time she was at her doctors Lisa got tested for Hepatitis C which the blood-borne virus that affects the liver. As it turns out Lisa has Hepatitis C and significant liver damage, because she most likely contracted the virus from that transfusion more than 30 years ago. I'm telling you this because my dissertation research compares the effectiveness of narratives, or stories that are similar to Lisa's with statistical information, which is what's typically seen in health related messages.

Prior research suggests that narratives may be one effective way of conveying this type of information. One reason is because narratives tend to be more easily comparative with our own lives, but as you can see a lot of health messages still rely on numbers to make an impact. I'll give you another example related to this.

So adults who were born between 1945 and 1965 are five times more likely to have Hepatitis C than other adults. Also those who are born between those years as you can see make up 75 percent of the people who have Hepatitis C. And the CDC estimates that of all the people who have this virus, up to 75 percent of them don't know because they haven't been tested. As you can see these numbers can help show you what a big problem something is, but on the other hand they can be hard to make sense of, especially if the same number repeats for different things, like 75 percent. It can also be hard for people to relate to those.

So, to account for this, my research includes a narrative like Lisa's story along with statistical information like I told you, but it also includes a third format that pairs both of these together. So, for instance after hearing that people in her age group are five times more likely to have Hepatitis C than other adults Lisa decided to get tested for this blood-borne virus. I'll let you fill in the rest, but as you can see this kind of lets you have the best of both worlds and at the end of the day this might be the most effective way to convey this type of information. So, the implications from this research are really exciting because they could help influence future message designs and in turn help people like Lisa to change their story. Thank you.

[Applause]

[Speaker: Scott Weber] Thank You Kristin. 

[Speaker: Scott Weber] Our next presenter—and our last presenter—is Van Anh Nguyen, her title is "Clicking Wires Inside a Biological Bomb Targeting Cancers Weak Links." Her advisor is Donald Major from the Department of Pharmaceutical Sciences. She's a relentless sampler of ethnic food, she was born in Russia—I think—and enjoys computer programming, psychology and fashion. Ready, set, pitch.

[Speaker: Van Anh Nguyen] Imagine yourself being strapped to a time bomb like the one you see in the picture on the left. You know that if you took out certain wires to stop the bomb from exploding and you know that if you do the in the wrong order, or touch the wrong wires the clock might start ticking a little faster. What are you going to do? Fortunately, I don't do this proposes, but my research pertains to something equally complex and scary, a biological bomb called cancer.

I wish I could find a cure for cancer, but over the time scientists realize that one solution fits all approach does not exist for cancer, just like you don't expect to find one perfect way to defuse every single bomb attack, we should not expect to find a magic therapy that will work for every cancer type or even subtype. So, does it mean that we should all just give up? Absolutely not! It means that every cancer requires a tailored approach, but I believe that the more you know about your enemy they're more likely you are to win the war. What I'm saying is that—you want—if you want to find the best treatment strategy for your cancer of interest, you would start by collecting all available information about the processes or wires that drive the functioning of your cancer cell.

My work is focused on Non-Hodgkin Lymphoma, which is the blood cancer. I'm interested in knowing what patients with different subtypes of the disease do not respond in the same manner if given the same treatment. My analysis points out that the differences were observed could be partly explained by the ways or subsets a wired, which changes all together how we should treat them. But first I need to know the structure of this biological bomb and what they're made of. So, I put together a puzzle—or what we call a network—that paints a comprehensive picture or what's happening inside them for myself, very much like the diagram on the right. This picture would be slightly different depending on which genetic alterations were introduced in each subtype, that cause a normal cell to turn to a cancer cell. Therefore, it's the most appropriate drug treatments for each subtype will also be different, and we can determine that by applying techniques that are based on mathematics and biology.

However, identifying most promising wires to clip is no longer enough. Cancer therapy has become increasingly complicated due to understanding that more often than not, patients require a multi drug regimen to overcome the devastating disease. We need to know which combinations of wires will merely slow down the clock and which one can actually terminate the bomb. This is where mathematical modeling comes into play, it allows us to predict what, when, and just how much to give to patients, before we go into clinical trial. Doing so can significantly cut down the time that it takes to develop successful therapies, they can save lives of thousands of patients.

So, we've come a long way in understanding in battling cancer and we still have a lot of work ahead of us but I'm confident that we will get there one wire at a time. Thank you.

[Applause.]

[Speaker: Scott Weber] Thank you so much. Ladies and gentlemen, we have just enjoyed 15 incredible presentations and I'm sure you enjoyed them as much as I did. Let's give another round of applause to all of our presenters. Our judges are working on their last evaluation and when they're done that we're going to allow them to step out of the room and you can do that whenever you're ready, so they can begin the deliberations, and I think they're gonna have a tough job. I would point out that we've retained Price Waterhouse to help with the [laughing] sorry I just popped up you know. But while they're doing their fine work and tough work remember what we said at the beginning of this presentation and an event that we said that you and the audience are going to have a chance to be a judge as well.

So I think what we're going to do is we're giving you time to get your devices out, turn them on (now it's appropriate) and pull them up and pretty soon I'm going to give you a signal when you have about three minutes we'll open the voting for about three minutes. The web addresses as you've seen up there, I'm not going to try to spell it out for you and everybody ready to vote? So you have time, I don't want to start too soon, I don't hear any objections so I think we have to say ready, set, vote!

[Speaker: Scott Weber] Our next presenter is Xiaonan Tai. Her title is "Where do trees die?." Her advisor is Scott Mackay in the Department of Geography. Loves chicken wings and to balance that, loves to hike and bike along the Niagara River. Ready, set, pitch!

[Speaker: Xiaonan Tai] Our forests are dying. The recent warming and reduced rainfall are killing trees. Without sufficient water, trees could not function properly and are more likely to be affected by disease, insects, and eventually die. The questions remain about where do they die and why? Do trees die randomly by chance or if there's a reason behind? That is the central question of my dissertation.

Now, let's take a look at this bird-view photo taken by flying a drone over my study area in the state of Wyoming. We can see that some trees fell apart after they died and create this open ground and some trees are close to death with their canopy turning grey or brown and the other trees remain green and happy. Notice the spots where the cluster with and trees. That pattern suggests that trees do not die randomly, there is a reason behind. What could be causing it? What could be the underlying factors? I find a number of things, soil types, plant differences in micro-topography—that is the subtle fluctuation of land surface.

Imagine that winter rains, some local depressions tend to collect water and remain wet for a longer time while others become dry pretty fast. Some soils can hold more water and some plants may grow deep root allowing them to access additional water. In order to understand how those factors combine to influence the amount of water that a tree can get, we need to know the movement of water laterally across the landscape and vertically from soil to plant. How do I deal with this complexity?

As a geographer, I was trained to integrate multiple disciplines by relying on knowledge from geology soil physics in plant biology. I built a computer model that can capture those factors and predict the water object for every individual tree across the landscape. This model will be combined with sophisticated observations of soil and plants to help us understand the pattern of mortality that we see here.

Ultimately, my research will predict locations with vulnerable trees in a changing environment and help us better protect our forest, which is so critical for all the lives on earth. Thank you.

[Applause]

[Speaker: Scott Weber] Thank You Xiaonan.

[Speaker: Scott Weber] Our next presenter is Nadav Weinstock. His title is "Understanding Krabbe Disease." His faculty advisor is Laura Feltri, in the Department of Medicine and Biomedical Sciences. He—I don't know the circumstances—but apparently broke both his arms when he was a child at the same time, yeah. Loves squash, the sport, not the vegetable—which I think is awesome—and hopes to travel to outer space sometime in the future. So, ready set pitch.

[Speaker: Nadav Weinstock] Parents love for their child is powerful. That love is limitless and unconditional, and if a child gets sick a parent's love perseveres. It's that love that encourages me to become a pediatrician and adjoin in the worldwide effort to cure childhood disease.

I study Krabbe disease, a devastating neurological disease that affects babies. Some of you may have heard of Krabbe disease from local Hall of Fame quarterback Jim Kelly, and his son Hunter. When Hunter was just three months old, he was diagnosed with Krabbe and doctors told the Kelly family there was nothing they could do. Hunter fought bravely but like all children with Krabbe, ultimately passed from his disease. Today, more than 20 years after Hunter’s diagnosis, not much has changed in the field. There's still no cure for children with Krabbe and there exists a fundamental gap of knowledge regarding what causes the disease and why our treatments aren't working.

To help you understand Krabbe, I want you to imagine your own life. If the garbage man never showed up, garbage would accumulate, first in the kitchen and in the living room, then the whole neighborhood. Something very similar happens in Krabbe. Patients are missing an enzyme and without that enzyme, cellular waste accumulates, causing disease. The problem is we don't know where that toxic waste is coming from. And if we don't know where the problem starts, how can we fix it? My research project focuses on answering that question by using a series of cutting-edge genetic tools that my mentor and I helped create. We're now able to pinpoint precisely where that toxic waste is coming from.

Shortly after starting our experiments we made a meaningful discovery, we found that one of the cells that contributes to this disease, the cell type known as the Schwann cell. Interestingly we found that Schwann cells can cause disease even when the surrounding cells are healthy. This last point is important, it contradicts what we thought we knew about the disease for years. We thought that any sick cell could be helped by a healthy donor cell. That was the basis of our treatment options. Children would receive bone marrow transplants from healthy donors. Our data not only suggest that Schwann cells may contribute to the disease, but also may explain why our therapies aren't curative and with this information we can design better therapies that target the underlying problem.

Every year I meet dozens of families with children affected by Krabbe, their lives were turned upside down overnight. One moment they had a healthy child with their whole life ahead of them, then the diagnosis came and their lives are changed forever, but the story doesn't have to end here. With our research, we're closer to finding a cure than ever before. Thank you.

[Applause]

[Speaker: Scott Weber] Thank you Nadav.

[Speaker: A. Scott Weber] Our next presenter is going to be Chong Zhang and the title of the presentation is “An Enzyme to Remember With No Strings Attached,” the faculty advisor is James O'Donald in the department of pharmacology and toxicology. She loves, apparently, bad jokes, Wikipedia, and we're super excited to have her here as well. So why don't you come up on stage. And ready, set, pitch!

[Speaker: Chong Zhang] Remember one time when you walked out of a shopping mall, went into the parking lot, and for a second you forgot where you parked your car? Once or twice that's okay, but when this keeps happening or even worse, it comes to a point where you can't find your way home, and that person is probably going to be diagnosed with memory disorders. As unfortunate as that can be there are no treatments. Only a few FDA-approved drugs have shown to relieve the symptoms but none of them slow down or reverse the disease progression. Now come to think of it, memory disorders may result from a wide range of causes, so it is difficult to pin down to a specific drug target based on that. Alternatively, it's not a bad idea to think about the memory process itself and that's what I'm interested in.

Decades ago a signaling molecule called cyclic AMP was found to be critical to the memory process. And this cyclic AMP also known as CAMP is controlled by an enzyme called PDE4. Back then a drug was found to inhibit PDE4 and improve memory, both in lab animals, which we work with, and humans. Exciting right? But this drug also produced severe nausea and vomiting, and for years it seemed impossible to separate the beneficial effect and the side effect.

For my dissertation project I've been working with a biotech company and a new class of pde4 inhibitors and specifically we targeted pde4-D which is a small group of PDE4. Now let's take a look at this image here. Think of when you are trying to wash your hands. On the left the old drug turns the faucet all the way up, gives you a big stream of CAMP, it gets the job done but you also end up splashing yourself just like some brain areas are flooded. And on the right, the new inhibitor the targets pde4, gives you just the right amount of water flow and lets you efficiently wash your hands. You probably figured out by now less is more as I mentioned before, we work with lab animals.

How do I know it's the same for humans? Well for starters, we made a mouse model that expresses humans heightened PDE4D and I've shown that this new inhibitor improves memory in this mouse model. And more importantly without causing any concomitant nausea and vomiting. I've also looked at the actual changes in the proteins and the activity level of the brain that are caused by this drug. And all those information tells us this may indeed be a better functioning brain. My data supported phase 1 trials in humans in which this new inhibitor first in his class showed promising results. And this brings hope to not only people with Alzheimer's but also those with other memory deteriorating conditions, even like aging, thank you.

[Applause]