Welcome to From the Spectrum Podcast. This is a podcast about autism. It is my
goal to explain what is autism. I plan to use a mixture of scientific literature,
personal experience, and opinion. With opinion, I will explain why. I feel the
way I do and give examples. I will provide links to various references for each episode.
For each episode, we will discuss various aspects of autism. For today's episode,
it is my pleasure to announce the guest, Dr. Leanna Hernandez. Dr. Leanna Hernandez is an
assistant professor in the Department of Psychiatry and Biobehavioral Sciences at UCLA and a member of
the Center for Autism Research and Treatment, or CART, the Center of Neurobehavioral Genetics and
the Brain Research Institute. Dr. Hernandez also serves as a co-director for the genetics,
genomics, and informatics core for UCLA's Intellectual Developmental Disabilities Research Center.
In addition, Dr. Hernandez directs the Hernandez lab at UCLA, where they examine genetic and
neurobiology of autism, schizophrenia, and other related psychiatric disorders. Our discussion
includes genetic variations and brain connectivity in autism, oxytocin and oxytocin receptor gene,
sex and diagnosis differences in autism and brain connectivity, and the future of autism research.
With the sex and diagnosis differences, you have autistic boys, non-autistic boys, autistic girls,
and non-autistic girls. So, four comparison groups. As you hear, Dr. Hernandez explain this
connectivity. Think about autism, what you know about autism. Remember the social communication
and interaction challenges and the restricted repetitive behaviors, the preference for routines,
sameness, and those preferences for restricted, fixated interests that are perfect in intensity
or focus. You know the DSM uses abnormal, but to say abnormal with interest, intensity, or focus,
is wrong by them. Now, think about how the biology that gives us autism provided those
behaviors, those routines, the sameness, and so-called restricted behaviors. They are safe and predictable.
The biology that gives us autism creates a chaotic outside world, and this connectivity gives us poor
adapting skills. With the poor socialness and restricted behaviors, we have limited adaptive
responses, and an unpredictable chaotic outside world requires adaptive responding. The biology
that gives us autism allows us to be comfortable within ourselves, and that can be, that can be a
path for finding and developing superpowers. And now, my discussion with Dr. Leanna Hernandez.
Dr. Hernandez, thank you for joining. Why don't you start by taking us to the moment you realized
autism was going to be a part of your professional life, and take us all the way up to the present day.
Sure. So, I first started working in the field of autism after graduating from college with a degree
in psychology, and I started working as an in-home aide for kids with autism. At that time, I got to
know a lot of the different families and the challenges that they were facing, became familiar
with many of the different behavioral symptoms associated with autism, and just became really
interested in it more generally, and really fell in love with the kids and families that I was working
with. After that, I decided that I wanted to learn more about the brain and brain development in
general. I've always sort of been interested in development, and so I went on to work as a research
assistant at UCLA in a lab that collected MRI scans, so magnetic resonance imaging scans of the brain,
during childhood and adolescence, both in typically developing kids and in autistic males and females.
And so from there, I then went on to become really interested, obviously, in brain development,
and I learned more about the genetics of autism, and went on to do a PhD in neuroscience also at UCLA,
where I studied the effects of different genetic variants on the oxytocin receptor gene and how
they're related to brain function and connectivity. After that, I continued to be interested in the
genetics of autism and did a postdoc at UCLA again, really focused on psychiatric genetics, and began
to investigate genetic variants associated with autism through genome-wide association studies,
which is some of the work that we continue to do today.
Oh, wow. Okay. Tell me about the creation of the Hernandez lab.
Yeah, it's very exciting. So we just opened up our doors in December of 2022. So I currently lead a
small group at UCLA in the Department of Psychiatry in the Semmel Institute. And so our work really
continues to focus on understanding brain development, not only in autism, but also in other
related childhood neurodevelopmental disorders, including psychosis and ADHD. We're also very
interested in some behavioral symptoms that sort of cross-diagnostic boundaries. So for example,
issues with sleep or sensory processing. And so these are some of the things that we're continuing
to investigate. We conduct MRI studies, and we're also interested in identifying the genes that might
be associated with some of these different behavioral traits. Okay. So something that interests me is
the downstream effect of that might be autism, or it might be OCD, or it might be schizophrenia,
etc. Could you briefly explain maybe what is known about what causes the differences in the disorder?
Sure. Yeah. So a lot of the different neurodevelopmental disorders that you just mentioned are
highly polygenic. And so what polygenic means is that there are many genetic variants across the
genome that are associated with those different disorders. So for example, in the case of autism,
it's hypothesized that hundreds of genes across the genome are associated with the disorder.
Now, the genome-wide association studies that we've performed so far haven't identified all of
those genetic variants. The identification of those variants is really a function of the size of
your study, the sample size. So what we know is that some of the genetic variants, as you mentioned,
that are associated with autism might also be associated with ADHD or schizophrenia. And this
would indicate what we might call a positive genetic correlation, meaning that the same genes
are influencing two traits. And so there are some of those variants that will impact
multiple traits. And then of course, there may be others that are specific to a particular
neurodevelopmental disorder. And so that area of research is still really ongoing, identifying
those shared and unique genetic underpinnings of the different neurodevelopmental disorders.
It always seems like there's a lot of variability and moving parts coming
funneling down into the individual. Let's start with one of your earlier research papers released
in 2017, if you don't mind, in molecular psychiatry. Take us through what questions were asked or
how was it determined. You mentioned earlier, as you're in your education development,
studied oxytocin receptor quite early. And then was just around that time frame or
let's just walk through that paper. Okay, sounds great. Yeah. So this is a paper
focusing on genetic variants, common genetic variants on the oxytocin receptor gene. And so
what we're looking at here is single nucleotide polymorphisms or SNPs. And so these are common
genetic variants that occur across individuals in the population. They're very common. So by
definition, they occur in at least 1% of the population. And there are variations in a single
base. And so you can have somebody who might have an AG genotype, GG or AA. And so basically,
we're looking at differences between people who have these different genotypes at a specific
genetic variant. And so here we wanted to focus on variants on the oxytocin receptor gene. And
we chose that gene for a couple of reasons. First, because there had been animal studies that
showed that there are differences in oxytocin receptor gene expression in subcortical brain
areas that are involved in reward and social processing. And so some of the really foundational
work in this area has been done in animal models, where they found that, for example, in prairie
voles, which engage in high levels of parental behavior and are monogamous, if you look at
brain slices from prairie voles, which you'll find is really dense staining for the oxytocin
receptor in these subcortical reward-related brain regions, including the nucleus accumbens.
Now, you can contrast that with, for example, the meadow vol, which lives in solitary burrows,
and is non-monogamous. And what you'll find is much reduced staining for the oxytocin receptor
in that nucleus accumbens brain region in those meadow voles. And so that's, you know,
sort of an interesting starting point. Some animal work showing that there might be differences in
gene expression in this brain area in these two species that are quite different in terms of
those their social behavior. There had also been some studies suggesting that there might be a link
between different genetic variants on the oxytocin receptor gene and autism, so some family-based
studies. Although I do want to point out that more recent genome-wide association studies
haven't found a link with the oxytocin receptor gene. So a lot of the work that we were really
doing, as you mentioned, this was back in 2017, was more grounded in this, you know, animal work,
which had shown an association with social behavior, parental behavior, and bonding.
And so what we did there was we looked at four different genetic variants on the oxytocin receptor
gene, and we made an additive score across those different genetic variants. So how many oxytocin,
how many autism-associated, you know, alleles does a person have in adding them up across those four
different genetic variants. What we then wanted to do was to look and see how a person's sort of
additive genetic liability for autism on the oxytocin receptor gene might be related to brain
connectivity. And there we were really interested in, again, connectivity of reward-related brain
regions, specifically focusing on the nucleus accumbens. And so I know you've talked in some of
your previous podcasts about some human work that has shown that there may be differences in
nucleus accumbens activity in autistic people when viewing, you know, smiling faces, different sorts
of social rewards. And so that was sort of the basis for this work as well. So what we did is we
had about 40 autistic children and non-autistic children come and do an MRI scan. And what we
did was we looked at connectivity of the nucleus accumbens with different brain regions. And so how
this works is that you would take a seed, a region in the nucleus accumbens, and you extract
brain activity from that region. And then you look to see how that brain activity is
correlated with every other region of the brain. So are there brain areas that are increasing their
activity in synchrony with the nucleus accumbens? And also you can identify brain areas that are
that are sort of anti-correlated, right? Where the nucleus accumbens activity is going up and the
activity in these other brain regions is going down. It's like a seesaw. Yes. Vision it. Yes.
And so what we did was we looked to see, you know, first, what does this connectivity of the nucleus
accumbens look like in our autism group and in our other group? And so what we found was that, you
know, using this seed in the nucleus accumbens, we found really robust connectivity between this hub
of the reward network, the nucleus accumbens, and other subcortical reward-related brain regions,
the frontal cortex. And then we also saw some negative connectivity, so anti-correlated activity,
with subcortical brain regions like the thalamus and also visual cortex.
In autistic groups or the typical groups? In general, in both groups. In both groups. Yes. We
actually did look at the differences also between the autistic group and our typical group. And what
we found was that the typical group had more connectivity between the nucleus accumbens
and an area called the precuneus, which is thought to be really important when sort of thinking about
the thoughts of yourself and others. It's the hub of a network that we call the default mode network,
which I'm not sure if you've discussed yet already on your podcast. Not yet. Just briefly. Okay, great.
So from there, what we did was we really wanted to see the impact of these oxytocin receptor
gene variants on this brain connectivity. So we want to see how is connectivity changing as a
function of increased dosage on this particular gene. And so what we found was that in our autism
group, having more genetic variants associated with autism on the oxytocin receptor gene,
was associated with reduced connectivity between the nucleus accumbens and other
subcortical brain regions, including the cate, putamen, and also frontal brain regions in the
anterior cingulate. So the dorsal striatum, cate and pudiman, for the listener, I've discussed
this. That's more of like a what I know it as stimulus responses. Sure. Yeah, it's involved
sort of in, you know, implicit learning and your right stimulus response. Correct. Okay. I've talked
a lot about stimulus responses. So I just wanted to make mention of that. Yes, perfect. And so what
was interesting is that we found a quite different pattern in our other non-autistic group. So
in non-autistic individuals, what we found was that having more of these, they still have the
autism associated alleles, right? As I said, these are quite common genetic variants. So even in the
non-autistic group, what we found was that having more autism associated variants on the oxytocin
receptor gene was associated with increased connectivity between the nucleus accumbens
and regions in the frontal cortex, and particularly the frontal pole. And so we were sort of curious,
you know, what is this difference in connectivity? What does it sort of mean? And so what we did was
we extracted the connectivity values between that nucleus accumbens and frontal cortex,
and we said, okay, what sort of behavioral measures might this be related to? And so we took that
activity and we looked at its relationship with scores on the social responsiveness scale or SRS.
And so this is a parent-report measure of autism associated behavior. It is, you know,
adequate for use both in autistic and non-autistic groups. A very popular instrument, too,
during the autism assessment. And so what we found was that in this non-autistic group, this increased
connectivity between the nucleus accumbens and frontal brain region was actually related to
lower scores on the SRS, indicating more sort of typical behavior, less autism associated symptoms.
And so we took that to mean that that might be sort of a compensatory mechanism, this increased
connectivity between the nucleus accumbens and frontal cortex, that, you know, when a person
might have more autism associated variants on the oxytocin receptor gene, the extent to which you
can sort of up-regulate this connectivity between the nucleus accumbens and frontal cortex might sort
of buffer and, you know, result in more typical social behavior. Yeah. Kind of the prefrontal,
my vision of it is, you know, I always say, it quiets things so that we can properly evaluate
things. Right. Yeah, that's a big role of the prefrontal cortex is sort of top-down modulation
of some of these subcortical brain structures that we were just talking about. So that's a big
finding that difference. Whenever you first saw the total number of Ls, I'm gonna sort of, I got
that right, they seemed to me like they were pretty similar. Is that the population, has that 1%,
is that from the total, so you're saying the total number of autism associated variants
between the two groups? Yes. Yes, they were very similar. That's right. As I said, these are very
common, you know, everybody has these single nucleotide polymorphisms, these SNPs. And so they
were present in both groups. Okay. So with the, with that SRS, what did that inform you or what,
what did that lead to as far as what was the next step here? The next step. Yeah. So,
so what we found was this relationship with specifically the social cognition sub-scale
of the SRS, which makes a lot of sense given what we know about the role of the frontal cortex in
cognitive functioning. And so the thing about the study that I just mentioned is that it was
performed in two groups of largely male children. And so as you know, there's a large male bias in
the diagnosis of autism. And so, you know, we sort of started with this group of mostly male
individuals. But what we really wanted to do was to move on and also look at whether there might
be sex differences in the effects of these oxytocin receptor gene SNPs on brain connectivity.
And so in the next study that we did, we worked with the Gendar Consortium, which is a group of
researchers at different universities across the US who worked to gather a large neuroimaging cohort
of girls with autism and without autism. And so in our next study, what we did was a similar set
of analyses, but this time looking at sex differences in the effects of the oxytocin receptor gene on
reward network connectivity. Yeah, this is wonderful data. What comes after this is just
wonderful data, I think, in the role of autism. Before we get into the data, can you explain to
us about Gendar? Sure, yeah. So this was a collaborative effort across a couple of different
research institutions in the US in order to recruit and collect data from a large cohort
of autistic girls. And so the four different sites for Gendar and Gendar stands for gender
exploration of neurogenetics and development to advance autism research, just so everyone knows
what that stands for. But so the girls were recruited and participated in MRI scanning at four
different sites at Harvard, Seattle Children's Hospital UCLA, and also Yale. And so the data
came from these various sources and really gave us the opportunity to examine what was when this
data was published, you know, the largest study of neurogenetics in girls with autism.
There's some powerhouse universities there too involved. Yes, absolutely.
Let's talk about some of those scannings or the scanning and the connectivity with this data.
Sure, sounds great. So similar to the previous study, everybody came in and had an MRI scan.
These MRI scans are done, I should have mentioned, while everybody is at rest. And so
people come in and have an MRI scan. But what they're actually doing is just looking at
a little black sort of crosshair plus sign on a white screen. And they're told that they can
just let their mind wander while we take pictures of their brain. And so we use those pictures as
I mentioned in order to look at these co fluctuating signals across different brain areas. And so here
again, we're looking at co fluctuating symptoms between the nucleus accumbens that have the reward
network and other brain regions. Okay. And some interesting findings, I think, is how the autistic
girls one differs from the autistic boys, the similarities maybe between autistic girls and
the typicals. Right, right, right. So what we found was that similar to what we found just
generally for connectivity in the male groups that when we looked at what other brain regions the
nucleus accumbens was connected to was really robustly connected to other reward related brain
regions and also frontal cortex. And then again, again, we found those negative associations
with the thalamus and visual areas. And that was both in autistic girls and non autistic girls.
So the next thing that we wanted to do was to look to see whether there may be any differences
between those two groups. And we actually didn't find any differences just looking at, you know,
connectivity of the nucleus accumbens more generally. And so the next thing that we did was to look at
how these oxytocin receptor gene variants might influence this connectivity. So what we found was
that in the non autistic group, having more autism associated variants on the oxytocin receptor gene
was associated with increased connectivity with frontal brain regions. While in the autistic
female group, we actually found that more of these oxytocin receptor gene variants was associated
with increased connectivity with other sub cortical brain regions, including the caudate and the
thalamus. And so like we mentioned before, these are two brain regions that are very important
in implicit learning. And so we wanted to see what this connectivity might be associated with.
And again, we looked at associations with other behavioral measures. And what we found was that
higher connectivity between the nucleus accumbens and the sub cortical areas was associated with
higher scores on the ADOS repetitive behavior scale, which we thought was quite interesting.
That is interesting. It kind of leads me to a question of, well, maybe one, what draws these
individuals, these autistic girls into an assessment? And how, what are their assessment
results look like to receive that diagnosis? Right, right. I mean, so overall, we did find that the
autistic girls had higher SRS scores relative to the non autistic group. But, you know, as you know,
there are, there's sort of ongoing research in terms of the diagnostic criteria that goes into
identifying girls and boys with autism. And so one thing that you may have talked about already
is the female protective effect or this hypothesis of a female protective effect in autism,
which sort of suggests that it's possible that females may require a higher number of genetic
variants or environmental factors to occur in order to sort of express the autism phenotype
relative to males. So that, you know, that females would require relatively more of these
different factors in order to actually go ahead and get a diagnosis. Okay. There, it appears
that their social motivation is much different than autistic boys and pretty similar, if not
equal to or greater than the non-autistics. And something else that I was wondering is
if that social motivation is actually above the normal where they might need more affinity or
more social interaction. And if that is a result of the biology that gives them autism or what leads
them into the assessment. Yeah, that's really interesting. You know, I haven't done a lot of
research myself on differences on the SRS or social motivation in girls with autism, but I think
that's a really interesting point. Yeah, okay. It's also the question about how girls camouflage
or mask. Right. Yeah, I think that leads in really well to actually the next finding. Maybe I should
talk a little bit more about the next finding in the paper. Okay, great. So the next thing that we
wanted to do was to compare autistic females and autistic males. So how might this, you know,
differences in the oxytocin receptor gene be differentially modulating brain connectivity
in these two groups? And so what we found was that relative to autistic males, our autistic females
showed up regulation of connectivity between the nucleus accumbens and the frontal brain region.
And so this was really exciting to us because there was, you know, really a lot of overlap
between this frontal brain region that we found was upregulated in the autistic females and the
brain region where we had previously found in the 2017 paper that higher connectivity in males was
associated with lower SRS scores. So what we did again here was we took connectivity between the
nucleus accumbens and this frontal brain region and we plotted them as a function of the SRS
in our girls with autism. And so what we found was that really mirroring the results from 2017,
again, having more connectivity between the nucleus accumbens and frontal brain regions
was again associated with lower scores on the social responsiveness scale.
Sort of suggesting that there might be this sort of neurobiological compensatory mechanism that
may facilitate some of this sort of masking behavior that you were just mentioning in girls
with autism, given that we're finding this increased connectivity between frontal brain
regions involved in cognition and cognitive control and these subcortical brain regions
involved in reward and social processing. Wow. That's quite the findings as far as recent
autism research and especially the gender differences. With those findings, how do you
anticipate that informing the assessment side or the instruments used for diagnosing autism?
I mean, you know, I think what it really indicates is that there are probably other
genetic and environmental factors that interact with the oxytocin receptor gene that cause these
that are associated with these sex differences. And so what those are, I think is still an open
question. And so I'm not sure how this might impact use of the SRS in order to and SRS is
not a diagnostic instrument, in fact, for autism. The ADOS and the ADIR, the gold standards for
autism diagnosis. But what it sort of suggests is one biological mechanism that might be sort of
facilitating enhanced social behavior in girls with autism. This female protective effect,
findings like that explains a lot. It explains a lot about just the recency of autism,
both the increase of SS or a diagnosis as we were down to like 1 in 36 or whatever. And then
just what we knew about that boy bias. Right. Yeah. So there's been some previous research
showing that, you know, there are differences in gene expression in males and females. This may be
one thing that also interacts with autism genetic risk differences in hormone levels,
differences in, you know, environmental inputs. And so there are a lot of factors, I think that,
you know, need to be investigated in order to better understand some of these sex differences,
and especially potential sex differences in the influence of autism associated genetic variants
on brain development. I do also want to mention that, you know, in this study, we were looking at
one gene, right, the oxytocin receptor gene. But there are actually many genes, as I mentioned,
across the genome that are associated with autism. And so more current research is taking
more of a sort of genome wide approach in order to look at genetic variants and how they might be
related to brain development. And so, you know, more recently, we've been doing things like
looking at polygenic risk scores for autism, which really add up. So the idea there is that you would
add up the sort of effects of different autism variants across the entire genome
to generate a single score. And then you could look at that and see how it's related to brain
structure and function across development. How easy is that to do? Is that sometimes
complicated per individual? So, I mean, there are a couple of steps. The first thing that you really
need is a very well-powered genome wide association study of autism. And so currently, you know,
our current GWAS of autism are still relatively limited in their power to detect the genetic
variants associated with autism compared to other psychiatric diagnoses, for example,
schizophrenia, where there are very large GWAS studies. And so, you know, we really need to
continue increasing our sample size in order to be able to detect all of these different
genome wide genetic variants that might be associated with autism. And then from there,
it's sort of a matter of having, as I mentioned, the well-powered GWAS, and then also having
genetics data of your own in another cohort. So at UCLA, we often collect saliva in order to do
genotyping from the participants that come in. And so when you have genotype data from your own
individual group of participants, you can sort of marry those two different sources of data in
order to make a score indicating, you know, genetic predisposition to autism in the data
that you have from your own unique participants. Well, that's my best grade insight. I'm glad,
I'm glad you shared that. That's something, that's information that is hard to come by for
the lay public, just that information. Something with the oxytocin is very interesting,
though, because of the everything it's attached to, both in the central and peripheral nervous
system. So one, I guess it seems like that would be hard to narrow down, but two,
the amount of roles it has seems like a great contender on that end.
Yes, it has a lot of roles. You're so right. So the oxytocin receptor gene, when it's bound to,
sort of through a cascade of events, ends up impacting intracellular calcium levels. And so,
you know, that can promote the release of different neurotransmitters. Oxytocin receptors
expressed on excitatory neurons can promote the release of glutamate, which leads to enhanced
excitatory neurotransmission. For example, in the hippocampus, you know, oxytocin has been found to
enhance excitatory synaptic transmission and also help with learning and memory. Oxytocin receptors
are also expressed on inhibitory interneurons, where they can influence the release of GABA,
which is the main inhibitory neurotransmitter in the brain. And so that is thought to be involved
with some of the sort of anti-anxiety effects that it has by working on inhibitory control in the
amygdala. And then in the prefrontal cortex that we were talking about recently, oxytocin can
influence both excitation and inhibition. So it definitely has many roles and also, you know,
the roles are sort of dependent on brain region as well. So it leads up lots of different potential
avenues for investigation, I think. Yeah, yeah. Oxytocin is a very fascinating molecule in our
body. After this data, what kind of information could you share about how somebody in the lay
public can find this information and kind of develop their understanding of this spectrum
now that this work spectrum has kind of opened up? Right. No, I mean, I think what you're doing
here is fantastic. Bringing, you know, scientists on to talk about their work. It's definitely a
challenge. You know, a lot of the work that we publish is in different scientific journals. It's
not always accessible to a lot of people. I think scientists are also trying to do a better job of
actually communicating with the public through social media and other means, right? I think also
since COVID, we've had a huge opportunity to record lectures and talks and presentations at
different universities and post them online. You know, going to the websites of different
autism centers and research groups are all things you can do in order to learn more about this area
of research. But I think what you're doing here is really fantastic. So happy to have been here.
Yeah, it was one of my it was one of the things that motivated me. It's having,
reviewing scientific literature, then bringing scientists on like yourself and sharing such
wonderful data. What are some of the things that you're currently working on? Yeah, so a couple
of things we're working on. One is again, these large scale genome wide association studies of
autism. And I am particularly passionate about performing that research in diverse populations.
And so a lot of the what we know about the genetics of autism and a lot of different
psychiatric disorders right now is really focused on European populations. And we also know that
what we find in these European populations might not always, you know, sort of be portable to other
other populations from sort of a precision medicine perspective. So your ability to predict
using genetics is impacted based off of the different populations you might be looking at.
And so what we really need is larger, more diverse, genetic studies of autism, as I mentioned,
in order to identify these different variants that might be so to see it in not just with autism,
but also with other, you know, co occurring issues, for example, sensory processing problems,
you know, mode motor related delays. And so there's a lot of room, I think, in order to improve in
that area. So that's one of the one of the areas that we're currently doing some research on.
And then another area is, you know, everything we talked about today is the impact of these
common genetic variants or SNPs on brain connectivity. But what's the mechanism through
which those those SNPs are actually influencing brain development, right? So we know that
genetic variation in these different SNPs can also influence gene expression. And so what we're
also working to understand is how these different genetic variants might impact brain gene expression.
And then how that gene expression in turn influences developmental trajectories during
childhood and adolescence. Wow. It seems like such a crucial time for that.
Yeah, it's really a great time to be doing this type of research, because a lot of these really
large scale data sets have recently become, you know, publicly available. None of this work
could really be done without the participation of the community. But, but yeah, it's a great
time for doing this type of work. A lot of the different genetic variants that we've been talking
about today, and, you know, the genetic variants identified through GWAS of autism, each individual
variant has a very, very small impact, a very small effect size. So in order to identify these
these variants, you really need very well powered large scale studies. And so I think we're sort of,
you know, we're in that era now where a lot of these studies are available. And I think it's
going to be great for facilitating our understanding of autism and lots of other disorders as well.
Yeah, it's something that makes me anxious and excited about
what happens next. What do you think autism is in 10 years? In 10 years, I hope we're working to,
you know, just understand the unique biology and needs of the individual, and that we're able to
wear helpful intervene earlier on before the sort of manifestation of really difficult and what
can be, you know, impairing symptoms and that we would know earlier on in development who is more
likely to go on to need, you know, more targeted interventions for some of the different symptoms,
and that our work in genetics and behavior and brain development can help to inform some of those
some of those findings. Yeah, absolutely. That's where it's happening. I'm thinking about
April 2024 communications biology from UCLA released a study on six week old,
and they followed them up to 12 months. And that looked that was some revealing data about how
the 12 month at 12 month old, they started developing autistic traits using an instrument. It wasn't an
ADOS, I don't believe. I can't remember. But studies like that, and then the intranasal
option of oxytocin seems like it has a lot of promise. It's very low risk, which is phenomenal.
It's very inconsistent, but it does show that to it does help some. And so that's, that's a huge step.
I agree. Yeah, I think this work really helps to it just inform our understanding of how variation
in human genetics can lead to variation in brain development and behavior. Everything that we talked
about today, all the individuals who participated were children and adolescents. And so I think your
sort of alluding to moving to younger ages is, you know, very timely as well. At this point,
a lot of that data, the infant data is still the sample sizes are relatively small. And so,
you know, that's one area that I think we need to work on increasing sample size there so that we
have lots of power in order to identify different associations. But it's definitely a really
interesting time to be working in this in this area, all the all the data from the
different modalities seems to be coming together, you know, the genetics, the neuroimaging and the
behavior. And I think that's really, really interesting and can be really informative for
our understanding of heterogeneity in autism and other and other traits.
Yeah, yeah, I think you that was that was very well said about different disciplines are coming
together and working on kind of a common goal. And that's going to really just accelerate information.
So that's very promising.
Well, I can't thank you enough for coming on and sharing this wonderful data and being so kind.
And just letting us know what to expect from you and the autism scientific community over the next
few years and everything looks promising. And maybe we'll just hold you up to that.
Yes, thank you so much for having me and thank you for what you're doing here, you know, spreading
spreading information and inviting me on it's been a great experience. And I know, you know,
a lot of people are learning from you and what you're doing here. And so I appreciate you and
and good luck moving forward. Wow, thank you. Thank you so much. I hope you have a wonderful day
and good luck with everything. You too. Thank you. If you're listening and enjoy the episode
or enjoy the podcast, please feel free to leave a review or rating. In podcasting, reviews, ratings
and downloads are huge. And I very much appreciate your feedback. You can contact me at info.fromthespectrum.gmail.com
and thank you for listening to From the Spectrum podcast.