We are the Association for Child and Adolescent Mental Health, or ACAMH for short. And this is ACAMH Learn. Well, I think the most important thing that has been established is that ADHD is highly heritable. And that high heritability is seen both in children and in adults. If we flesh that out a little bit more, then what we're looking at is that the heritability of ADHD in children and adults is about 70% to 80%. What that means for ADHD is that for an individual, on average, 3/4 of their phenotype of the ADHD can be explained by genetics, whereas another quarter is brought about by the environment. So, obviously, this is on average, and there can be a widespread between different individuals. If we're thinking about heritability, many people think about one gene and one gene being defective and causing a certain disorder, a certain phenotype. This is not what ADHD is like. In ADHD, most of the genetic variation, the genetic variants that are involved in ADHD, have a very small effect on ADHD risk. And it is really many of these genetic factors coming together in a certain individual that lies at the basis of their ADHD. So it is highly heritable, but the ADHD gene does not exist. Very importantly, the same genetic variance, the same genetic alterations that we see in people with a diagnosis of ADHD also lie at the basis of traits of activity, traits of attention that we see in the general population. So, again, there are no genes that are really specific to ADHD. It is more the amount of genetic variance, the number of genetic variants that a person carries that are linked to hyperactivity, that are linked to attention, that makes whether or not this person is at high risk for developing ADHD or not. Another important established fact is that dopamine neurotransmission is involved in ADHD, and that has shown has been shown in many different ways, from animal work to genetic studies. We are able to see that genetic or that, sorry, that dopaminergic neurotransmission plays an important role. Most probably, also neurotransmission to other neurotransmitters, for example serotonin and norepinephrine, is also involved in ADHD. Well, first to say that a lot of recent work has brought us progress in understanding the biology of ADHD. So it's really through international collaboration, through availability of the data internationally, people coming together and working together that we now have picked up a very high pace in starting to understand what ADHD is in a biological sense. So these are really good times in making progress in understanding the biology of ADHD. Just to give you an example, and one of the most-- what I consider the most important leads in the literature currently in terms of the biology, is from an international study on the genetics of ADHD. In this international study from the Psychiatric Genomics Consortium and the Danish iPSYCH Consortium, people brought together data on roughly 40,000 people with ADHD and 190,000 1,000 without ADHD to study the genetic variation across the entire genome of these people and then find regions that are involved in risk for ADHD. This study showed us that there are about 7,000 genetic variants that are involved in ADHD. So an estimation was made, how many genetic variants are out there for ADHD? And this number may be 7,000. Of those 7,000, the study identified 27. This doesn't sound much, but it is a very important first step. And it actually helps us to understand, to go more into understanding the biological pathways and the biological mechanisms that underlie ADHD. And what was shown in this study was that both biological pathways that are linked to brain maturation. So, for example, for the outgrowth of neurons during prenatal development, and pathways that are involved in the day to day functioning of synapses, so the communication between brain cells, are important for ADHD. So we seem to have a neurodevelopmental component and we seem to have a more acute, everyday functioning component that play a role in ADHD. Another important finding from recent literature shows that there is a strong overlap between the genetic factors that are involved in ADHD in children and in ADHD in adults. And that adds to the literature that really shows the continuity of ADHD from childhood to adulthood. Also, what was shown that there is a strong overlap between the genetic factors for ADHD and the genetic factors for other psychiatric conditions. And what that shows us is that the genetic factors that underlie psychiatry are not very specific. That is important information that helps us understand mechanisms and also helps us to understand the potential limits of using genetic information in the clinic. Last, but certainly not least, what was also shown in recent literature is that there is a lot of genetic overlap between ADHD and other types of diseases, like for example, obesity, but also even rheumatoid arthritis seems to be linked to ADHD in a generic manner. And this means that the processes that are involved in ADHD are also important for problems outside of the brain, like for example, in obesity or in rheumatoid arthritis. Well, first of all, I think what is very important is that we understand more of the genetic influences on ADHD. As I just told you, we have identified 27 out of potentially $7,000 genetic variants that link to ADHD. So there is a lot to understand here as well still. Also, with these studies that we're currently doing, we're only looking into one specific type of genetic variation. So extending these studies to involve other types of genetic variation will help us understand more of the genetic component, more of the heritability of ADHD. What I also find very important to address in upcoming studies is the integration of genetic information with other types of biological information. And here we can, for example, think of brain imaging of information about brain structure, about brain function that we would like to link. And especially, while studies are already out there that tell us that certain features of the brain are slightly different in people with ADHD than in people without ADHD, we don't necessarily know how the genetics of ADHD actually influences the brain and brings about the phenotypes that we see in the ADHD brain. So this links between the different levels of biological insight is something that is very urgently needed. Furthermore, as I told you in the beginning, ADHD is not purely genetic. So we can learn a lot about the biology of ADHD by also integrating studies of the environment. So how do environmental factors and genetic factors play together in causing ADHD? One additional outstanding question, I would consider the fact that so far, we have only concentrated on explaining ADHD risk. But we'd rather or what we would want to know also is whether there are other factors that are protective that make people resilient to developing ADHD. And more studies going into the biology of resilience, the biology of functioning in ADHD would be very important to carry out. Last but certainly not least, an area that needs to be addressed is the clinical use, the clinical usability of genetic findings for ADHD. I've talked so far much about mechanistic studies and mechanistic insight. And obviously, through these mechanistic insights, we may be able to better understand which patient may benefit most from a certain treatment. We could help improve treatments, make them more pathway, more mechanism based, for example. But the question is whether we can also use genetics to inform diagnostics. And this is still a question that needs much more work. So far, the explained variance, the information that is in the genetic data is too little to warrant use of genetic data in diagnostic settings. And also, I told you about the lack of specificity of ADHD-related genetic factors. Factors that may hamper use in the clinic. However, we know from other areas of medicine that genetic factors are started to be considered, and genetic factors for these complex diseases like ADHD is one. So there is a possibility that in the future, we can make the ADHD genetics also work for us in diagnostics. And this would be, of course wonderful, because it gives us another potentially more objective way of supporting a diagnosis of ADHD. So looking at into the future, I think these are areas that are to be addressed. What I find very important in going forward in ADHD biological research is also to hear the stakeholders, more of the stakeholders in such studies and give, for example, people with ADHD a voice in determining how and what the studies that are prioritised. [MUSIC PLAYING]