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01:40
good morning everyone it's a pleasure to
01:42
see you all here today my name is Paul
01:44
nurse I'm president of this university
01:47
Rockefeller University and I want to
01:50
warmly welcome you to our full parents
01:53
and science breakfast forum this is the
01:56
first of three lectures that we've
01:59
specially designed the parents this year
02:02
now this parents and science lecture
02:05
series is a resource for new city new
02:07
york city parents who are interested in
02:10
gaining new insight into child and
02:13
adolescent development what we're hoping
02:15
to do is to offer a forum where you can
02:18
learn about great science participate in
02:21
a dialogue and share your perspectives
02:24
all about raising children I
02:27
particularly want to thank the trustees
02:29
of the lubin Family Foundation some of
02:32
whom are here this morning and for
02:34
generously underwriting this second year
02:37
of this initiative it's really greatly
02:39
appreciated I also want to extend a
02:42
special welcome for those of you who are
02:45
visiting the University for the first
02:47
time and I hope that today's program
02:50
will acquaint you with this rather
02:52
extraordinary institution founded in
02:55
1901 as the first biomedical research
02:58
institute in the United States now since
03:02
then Rockefeller has made remarkable
03:04
contributions to biomedicine recognized
03:07
the world over Pratt's on your way into
03:11
the auditorium you noticed our new Nobel
03:14
Prize and Lasker Award wall it was on
03:18
your right as you came in it'll be on
03:20
your left as you go out now there's 23
03:24
scientists associated with Rockefeller
03:27
and were only a small institution who
03:29
have received the Nobel Prize this is
03:32
quite an extraordinary track record of
03:34
success I want to put that number in
03:36
perspective for you if Rockefeller
03:38
University were a country it will be
03:41
ranked in fourth in Nobel prizes in
03:45
medicine in chemistry in the world
03:47
behind the United States Britain and
03:49
Germany and actually ahead of France
03:52
which will be fifth
03:57
so also remarkably for of Rockefellers
04:01
23 noble or its received their prizes in
04:04
the past nine years so it's very current
04:06
but there are other metrics of
04:09
excellence I'll just mention a couple
04:11
over 20 Rockefeller scientists have
04:14
received the albert lasker award this is
04:16
the american nobel often known as that
04:19
for medicine it's frequently a predictor
04:23
of a future Nobel Prize and well over
04:25
half of our tenured faculty are members
04:28
of the National Academy of Sciences do
04:31
refer to your program books if you wish
04:33
to know more about this quite remarkable
04:35
University now today's program we have
04:39
with us several leaders in the effort to
04:42
advanced scientific knowledge about
04:44
autism spectrum disorders and also
04:47
several supporters and thunders of this
04:50
crucial work I want to particularly
04:52
recognize the Simons Foundation for its
04:55
commitment to autism research it
04:58
supports research here at Rockefeller
04:59
and many other institutions and Marilyn
05:02
Simon's is with us today great pleasure
05:05
to have her here and thank her for her
05:07
support in today's program which is the
05:12
autism enigma we're really very pleased
05:15
that dr. Catherine Lord is with us as
05:17
our guest speaker after her presentation
05:21
will hear a brief overview of basic
05:24
autism research from neuroscientist
05:25
Jerry fischbach who is a visiting
05:28
professor here at Rockefeller were very
05:30
pleased to have him here on our faculty
05:32
he also serves as a scientific director
05:34
of the Simon's foundations autism
05:38
research initiative following Jerry
05:41
Fishbach he his remarks heat Jerry will
05:45
moderate a panel discussion with dr.
05:48
Lord and with Rockefeller scientist nap
05:50
Hines are James and Marilyn Simon's
05:53
professor and 2,000 Nobel laureate Paul
05:56
greenguard our vincent astor professor
05:59
dr. heints and greengard worked together
06:02
on an autism research project here at
06:05
the University funded by the sign
06:07
foundation and after the panel
06:08
discussion I will then moderate
06:10
questions and answers from the audience
06:13
so it's a busy program I hope you're
06:16
hanging on to your seats it's my
06:20
pleasure to start it by introducing dr.
06:22
Catherine Lord who directs the
06:24
University of Michigan's autism and
06:26
communication disorders center we're
06:29
really honored to have her here today
06:31
please join me in welcoming dr. Lourdes
06:33
to the podium thank you thank you very
06:44
much for inviting me here and my goals
06:47
today are threefold one is to provide a
06:50
very general introduction to autism
06:52
spectrum disorders or asds some of you I
06:55
know more far more than I will ever know
06:58
about asds but some of you don't so I'm
07:00
going to start very simply second of all
07:03
is to introduce to you the science of
07:06
how we try to understand the behaviors
07:09
that characterize asds and then my
07:12
particular interest which is
07:13
trajectories and development that is how
07:15
children and adults change over time and
07:19
last I'm going to briefly touch upon
07:21
empirical findings about educational and
07:24
behavioral interventions with the idea
07:26
of leading us into the questions of what
07:29
is a SD and how does it respond to
07:32
different behavioral treatments and how
07:34
then my neurobiology help us figure out
07:37
what causes this and what we can do to
07:40
change it so as most of you know it
07:44
autism spectrum disorders are defined at
07:47
this point purely by behavior there's no
07:49
biological marker that will lets us do a
07:52
blood test or measure something and say
07:55
that a child or an adult has autism to
07:58
make things even more complicated asds
08:01
are defined by difficulties in three
08:03
areas social reciprocity communication
08:07
delay or deviants and restricted and
08:09
repetitive behaviors and what we've been
08:12
trying to do in the last few years is
08:14
figure out what are these areas what
08:16
makes them
08:17
obvious in some ways and yet so subtle
08:21
and others now asd at least some aspects
08:25
of asd really fall on a continuum so in
08:28
order to study asd we have to force
08:31
these continuum into categories but
08:36
really we know that the behavioral is
08:38
very the behavior is very and this is
08:41
just from a standardized diagnostic
08:43
instrument where these are scores so
08:46
from low to high high meaning more
08:47
abnormal and this is the cumulative
08:50
proportion of subjects these are all
08:52
children who are very young nonverbal
08:55
and equivalent in nonverbal skills and
08:59
these are typical children it just shows
09:00
you the range this is a hundred percent
09:02
so up to from twenty percent to a
09:04
hundred percent of kids with typical
09:06
kids have scores the very highest scores
09:09
were up to four whereas if we look at
09:11
kids with diagnosis of pdd-nos or mild
09:13
or autism we have much more variability
09:16
overlapping a little bit with the
09:18
typical kids and then we have kids with
09:20
autism without intellectual disabilities
09:23
and kids with autism with intellectual
09:25
disabilities what I want you to see here
09:28
is we can easily separate this group
09:30
from these groups but there is overlap
09:32
and if we need categories we have to
09:35
some degree force the categories and say
09:37
okay if you fall in here you have ASD if
09:41
you fall over here you don't have a SD
09:43
and then here are these kids that fall
09:45
in the middle now I'm going to try to
09:47
make this a little bit more real with
09:49
video tapes in a minute but we can make
09:52
reliable diagnosis of ASD down to age
09:56
two and maybe even younger and all the
09:59
way up through adulthood and we can
10:01
quantify the severity of ASD that is we
10:05
can measure how severe or how impacted
10:08
is a child's life by the behaviors
10:12
associated with ASD the trouble is that
10:15
really a prototype model which is sort
10:17
of like if you think about prototypes of
10:20
birds as sparrows and Robin's it
10:23
probably fits autism more than a linear
10:26
model that is we know a lot about kids
10:28
in here who have the
10:30
most clearly defined behaviors and we
10:33
can measure how different they are from
10:35
kids out here who have less clearly
10:37
defined behaviors and I can teach you to
10:40
draw this line right here if I want to
10:43
but this line isn't a real line between
10:45
autism and PDD I've just kind of made it
10:48
up because we have to figure out how to
10:51
quantify it so we can decide who has the
10:53
spectrum and we can decide how severe it
10:56
is but actually determining what are the
11:00
lines that are associated with biology
11:02
are not well decided in addition to make
11:07
this harder yes these are developmental
11:10
disorders that is they change with
11:12
development a child at two who has
11:14
autism does not look the same as that
11:17
same child will look when they're 10 or
11:19
20 or 30 years old a child who is for
11:23
with autism who is functioning at a
11:25
two-year-old level looks different than
11:28
a child who is for with autism who is
11:30
not intellectually disabled who's
11:32
functioning at his age level so we
11:34
always have to take development into
11:36
account in addition autism affects
11:39
development and I'll show you a little
11:42
bit in a minute how that might be but
11:45
for a child with autism who doesn't for
11:47
example ever have a friend they don't
11:49
get the feedback that friends give you
11:52
so the autism not only affects where you
11:55
start but it affects where you go now I
11:58
think this area is one of the greatest
12:01
areas of hope for treatment because if
12:04
we can change the experiences of
12:05
children with autism and not let them be
12:09
limited by their own disorder we may be
12:11
able to really change the trajectory now
12:15
in addition to that autism is defined
12:18
both by positive or abnormal behaviors
12:21
the things that you see immediately like
12:24
a child who is looking at their fingers
12:26
or smelling things or lining things up
12:28
or talking furiously about buffalo's but
12:33
it's also probably more importantly
12:35
defined by the absence or do munition of
12:39
normal social behaviors but that makes
12:42
the die
12:43
gnosis much more complicated because we
12:45
then have to know what is a normal
12:47
behavior in that context and many of us
12:50
have preconceptions about what normal
12:53
behaviors are that really aren't true at
12:55
all so in coming up with a diagnosis we
12:58
have to try to identify situations where
13:02
typical children do a very restricted
13:05
number of things so that we can see when
13:07
a child isn't doing typical things and I
13:10
put this slide up just because this is
13:12
from a summer camp with kids with autism
13:14
whom you who are not that different than
13:17
the kids i'm going to show you in a
13:18
minute or very little but if you look at
13:21
the very little ones you'd think i would
13:22
never imagine them eating pizza in the
13:24
rain in a summer camp what I'm going to
13:28
do now is show you just a few video
13:31
clips from a standardized observation
13:34
where we're trying to figure out how to
13:35
diagnose autism in two in toddlers and
13:38
what I'm going to show you first it's
13:41
just a short interaction between an
13:43
examiner and a child who's under 2 and
13:46
the first child in each set is a child
13:48
that we think or actually we know
13:50
because we've now followed them has
13:52
autism the second clip is a child who
13:54
does not have autism but has a language
13:57
delay and what I hope you will see is
14:01
that actually the differences are quite
14:03
subtle and are much more obvious when
14:05
you see the second clip that is see the
14:08
child that doesn't have autism when you
14:10
just see the child that does let's hope
14:13
this works so here the examiner is
14:15
teasing you and just seeing what happens
14:18
to this boy if you offer she offers on
14:20
the ball gun
14:22
oh and think about what isn't he doing
14:25
compared to this little boy who does not
14:27
have autism so in fact I know the
14:35
differences are not big but hopefully
14:38
there will be a theme here okay this
14:42
here she's blowing up a balloon letting
14:45
the balloon fly all over the room and
14:47
then she's going to pretend that
14:48
suddenly she can't get that balloon to
14:50
blow up so she's interested in what does
14:53
the child do to get her to blow the
14:55
balloon up or cheer her on as she
14:57
struggles with the balloon this is a
15:01
little boy that has autism and think
15:12
about what is he doing but what is he
15:14
not doing that you would expect a child
15:17
to those contexts and this is a little
15:21
ball with the language
15:26
Oh chadron one more time ya know what I
15:33
wanted you this is both little boys were
15:35
near her both little boys were moving
15:38
their bodies but there are differences
15:40
in how the first little boy and the
15:43
second little boy move their bodies and
15:45
the fact that the first the second
15:47
little boy looks right at her and
15:50
vocalizes even though he can't really
15:52
talk and gestures to her where does the
15:55
second little boy is actually trying to
15:57
use her to inflate that balloon so he
16:00
knows where that balloon goes so it's
16:02
not that he doesn't know what's going on
16:04
okay and then the last one I'm going to
16:07
talk over this because this is a little
16:08
bit long the examiner is and the mother
16:12
who's sitting over in the corner are
16:14
just going to ignore this little boy
16:16
he's been in the room with them for
16:17
about an hour is quite settled and
16:19
they're just going to ignore him this is
16:22
a little boy who has autism and i want
16:24
you to see what he does and again the
16:28
point is this is this is pretty subtle
16:30
we're looking more for the absence of
16:32
behaviors than the presence of abnormal
16:35
behaviors now in this setting the
16:44
average length of time when we ignore a
16:46
child for them to try to get our
16:48
attention is 15 seconds and we will go
16:56
for a minute which seems like a year but
16:59
my point is think about in this child's
17:02
life if for every minute or every five
17:05
minutes when someone isn't engaging him
17:08
if he doesn't engage them what does that
17:10
teach him about social development and
17:14
how does that affect his ability to get
17:16
information and listen this is a little
17:19
brown who is intellectually disabled
17:21
scooch amount maybe like the middle
17:23
between us let's see what his reaction
17:25
is to being ignored against and then you
17:27
can respond it so not autistic
17:52
that was busier with so my point is that
17:58
sorry this again is that that may seem
18:03
to you like we are like the fellow with
18:06
a microscope where we're obsessing over
18:08
tiny things but my point is these are
18:11
important things if a child is getting
18:14
radically different amounts of feedback
18:18
about from people and learning less from
18:22
people starting at 15 months or 18
18:26
months what does that do about brain
18:28
function and also what how can this
18:31
perhaps help us figure out what's going
18:33
awry now genetic studies of ASD began
18:38
with twin studies and what's interesting
18:40
about them are a number of things first
18:43
identical twins if you have a child with
18:46
autism who is an identical twin the
18:48
chances of the other child having a
18:50
autism are about sixty percent so much
18:54
higher than fraternal twins which is
18:56
problem is under ten percent and perhaps
18:59
under five percent so suggest there is a
19:02
genetic component to autism if you
19:05
include the broader phenotype that is
19:08
you include language delays high social
19:12
anxiety social aloofness than the
19:15
concordance or agreement in identical
19:18
twins for ASD like symptoms is ninety
19:20
percent so very high and this was the
19:23
start of autism genetics it was then
19:27
followed up by family studies that
19:29
suggested that if you have a child with
19:31
autism your chances go way up from say
19:35
one in a hundred and fifty to maybe one
19:37
in 20 or even higher of having another
19:41
child with ASD and your chances of
19:44
having a child with some kind of related
19:47
problem and that may be a language delay
19:49
that actually resolves itself are also
19:51
significantly higher now we'll hear more
19:54
from dr. fish back and I'm sure in our
19:56
conversations about them
19:58
ocular genetics that's followed up on
20:00
this but I think one of the important
20:03
behavioral things is that when people
20:05
took all of the twins of the twins study
20:08
so there were about 80 twins and they
20:11
randomly sorted them so instead of
20:12
matching them with their own twin they
20:14
match them with the twin that they
20:16
weren't related to it all and then they
20:18
looked at the pattern of differences in
20:20
verbal IQ between these randomly
20:23
generated to in pairs um this is the
20:26
range of a standard deviation and this
20:28
is this these outside lines are for the
20:32
twins that weren't related to each other
20:33
at all then you look at what is the
20:37
relationship in IQ between the kids the
20:39
twins that are their own identical twin
20:42
and it actually fits right in here with
20:45
the random distribution so what does
20:48
that mean it means that the genetics of
20:51
ASD are affecting autism spectrum but
20:55
there's still huge variation even with
20:58
identical twins in other factors like
21:01
verbal IQ so that you can see look at
21:04
this fifty percent of the population of
21:06
twins have a difference in verbal IQ
21:09
that's huge I mean it's over 60 points
21:13
so whatever is being transmitted is not
21:16
going quite along with verbal IQ now we
21:19
also know that within a population of
21:22
ASD we have incredible heterogeneity or
21:26
variability in language and this is just
21:28
a study we've done where we followed
21:30
about 200 kids from age 22 age 9 and
21:34
each one of these lines is a different
21:36
child learning language and you can see
21:39
this is normal this would be what normal
21:41
is there's everything from kids who are
21:43
doing extraordinarily well to kids who
21:46
are coming along much more slowly so we
21:50
have the case where we may have a number
21:53
of different ideologies we've got to
21:56
find these brain mechanisms that can
21:59
identity for all this all these
22:01
heterogeneity these differences in here
22:03
and I think what the twins remind us is
22:06
that even when we presumably
22:08
have the same ideology we can still have
22:11
heterogeneity we can still have a twin
22:14
who is highly verbal and can talk your
22:17
ear off and another twin who also has a
22:20
SD who is nonverbal now what does this
22:23
mean about treatment the most
22:27
well-established finding and behavioral
22:30
treatment of autism is that intensive
22:32
ABA results in improvements and this is
22:36
the most well-established lending form
22:38
analysed control trials these
22:39
improvements generally have been
22:41
measured in IQ and language scores and
22:44
results in improvements of about 10 or
22:46
20 points so that's great if you are say
22:50
have a verbal IQ I'm not trying to say
22:53
verbal IQ is the end of all of anything
22:55
but just because its measured of 70
22:58
going from 70 90 is incredibly important
23:01
if you have a verbal IQ of 30 going from
23:04
30 to 40 may make a big difference in
23:06
your life but it does not pull you into
23:09
normality on the other hand these are
23:12
very significant changes recently just
23:16
in the last five years there have been a
23:17
lot of very brief primarily parent
23:20
directed interventions around joint
23:23
attention those have shown smaller
23:25
changes they often involve just an hour
23:27
a week of working with parents but they
23:30
have shown consistent changes in
23:32
language attention and IQ in randomized
23:37
control trials there is also a huge
23:39
literature looking at very specific
23:41
kinds of behavioral plans and behavior
23:45
programs to reduce aggression to
23:47
increase communication that involve
23:51
doing very specific things and those
23:53
things are shown improvement so it's not
23:55
that we don't know anything but I think
23:58
we also realize that there are very
24:00
likely interactions between what the
24:02
child can do and can't do and
24:04
differences between children and also
24:07
differences in parents I mean somebody
24:09
just did a study showing that if you're
24:11
teaching a child by responding to their
24:14
initiations and you have a parent who's
24:17
very responsive your change you don't
24:19
change anything very
24:21
much if you have a parent who is not
24:22
very responsive you do so we need to
24:25
take into account the rest of the
24:27
environment now one thing I think we
24:30
have to remember though is autism is
24:32
very responsive to placebo effects now
24:36
the good thing is it means that hope and
24:38
whatever it is that gets to us when
24:40
we're doing interventions can really
24:43
make a difference on the other hand we
24:45
have to be very careful and this is data
24:47
from mystic RCT a randomized control
24:50
trial secretin and you can see these are
24:52
the kids who got the secretin these are
24:54
the placebo and actually this is scores
24:56
and irritability everybody went down and
24:59
in fact this was found in numerous sites
25:03
and I was part of it and actually was
25:05
sure something was actually happening it
25:07
was so exciting except that it was
25:10
happening for our control group just as
25:12
much as for the treatment group so what
25:16
I think I want to propose to you and to
25:19
get the neuroscientist to think about
25:21
today is that we need to understand what
25:24
goes awry and also what goes well and I
25:27
haven't talked about that very much nasd
25:30
as we plan interventions and as we try
25:33
to figure it out and we want to be very
25:34
careful that we're not trying to explain
25:38
a myth of what people thought autism was
25:41
50 years ago that is not really true in
25:45
addition it seems to me that we one way
25:48
to think about ASD is that it really
25:50
should be considered just along the
25:52
lines of like we would check for hearing
25:54
impairments or visual impairments it
25:57
should be a standard we should screen
25:59
for it but we also know that there are
26:01
kids who have multiple or all of us many
26:04
of us have multiple visual impairments
26:06
it's not just one thing it's multiple
26:08
things and all of those things need to
26:10
be addressed and treated and there is no
26:13
reason also that that should be
26:15
stigmatized I want to end just with a
26:18
note and again an example for you to see
26:21
just the variability in autism that I
26:24
think things are changing tremendously
26:27
in terms of changing the trajectories of
26:29
kids with ASD by starting early
26:33
changing social experience we can give
26:36
kids a whole different lease on life and
26:39
this is from our social group in
26:41
Michigan so this is produced directed
26:43
and written by them and I think what you
26:46
can think about here is sometimes I
26:48
would substitute the word ASD for Waldo
26:52
so hopefully this will play Oh welcome
26:59
to the where's father channel usually
27:03
usually mean nobody knows about all
27:07
those pastimes but we decided he's
27:10
always secretive but we decided to find
27:14
him and get an intimate look at his
27:17
personal life so here to enter me for
27:20
this interview is baldo himself where is
27:25
he first we'll know where you go all
27:29
right again so what I wanted you to see
27:33
is just that it is not that people with
27:35
autism have no sense of humor or no
27:38
creativity or no ability to work
27:40
together because this was film directed
27:42
and planned by them and I think the
27:45
point is we need to come up with models
27:47
that encompass everything from the
27:49
little boy that you saw flapping trying
27:52
to put the balloon in the researchers
27:54
now to this young man who's in regular
27:58
school and who sees himself as the next
28:01
marc forster or film director anyway on
28:04
that note let me thank you very much
28:11
hi I'm Jerry push back and I'm going to
28:15
moderate the panel but I'm also going to
28:19
give about 10 minutes of overview of the
28:22
biological and biochemical approaches
28:26
that are currently underway in studying
28:28
autism and the scientific director of
28:31
the Simons Foundation autism research
28:34
initiative and have been very interested
28:38
over the past two years and how to
28:39
approach this complex phenomenon through
28:45
laboratory science and I must tell you
28:47
right off the bat I'm become incredibly
28:50
optimistic this is a tough tough problem
28:53
the complexities we just saw a
28:55
clinically are multiplied when one tries
28:59
to approach this in the laboratory but
29:01
it is an exciting time in both
29:04
neuroscience and in genetics and I
29:07
believe that there is as much hope for
29:10
true insights about autism now than ever
29:13
in my scientific career of 45 years in
29:17
the laboratory so this is a valuable and
29:21
critical effort so Kathy went through
29:26
the definition of autism as changes in
29:29
social cognition changes in verbal
29:33
communication and changes in repetitive
29:35
and restrictive interests and I quite
29:38
agree that one must approach these as in
29:41
the full complexity and not trying to
29:44
explain all things by certain cellular
29:47
mechanisms but it is clear that the
29:52
autism is manifest through its action in
29:56
the nervous system and the brain the
29:59
human brain is I believe one of the most
30:01
complex objects in the known universe
30:03
it's about two and a half pounds but it
30:06
does have 100 to 200 billion cells and
30:10
the real complexity lies in the
30:13
connections between those cells in what
30:17
are called synapses because each cell
30:20
each of the 100 bill
30:22
in cells may make hundreds if not
30:24
thousands of connections with other
30:26
cells and that's not even where the
30:29
complexity lies the complexity lies in
30:32
the ability of those connections to
30:34
change with experience with
30:36
environmental input and with genetic
30:40
factors it's the plasticity of the brain
30:42
that offers its complexity but also
30:46
offers great hope for change and
30:49
recovery and education and therapeutics
30:52
this is a nerve cell it's like any other
30:56
cell in its outlines there's a nucleus
30:59
surrounded by a cytoplasm and a cell
31:03
membrane that keeps the cell intact the
31:06
genetic material is located in the
31:09
nucleus of that cell the DNA is packed
31:13
within the nucleus and instructions in
31:16
the DNA enable the manufacture of
31:19
proteins outside of the nucleus which
31:23
are distributed to all aspects of the
31:25
cell and it's these proteins that are
31:27
the building blocks of the cell that
31:30
ensure cell health and when there is
31:32
damage to a protein they lead to
31:35
disordered function the nerve cell has a
31:39
particular unusual shape it's polarized
31:44
that has a receiving service and a
31:47
communicating surface these genes in the
31:51
nucleus are what has been offered a
31:54
great deal of interest and increasing
31:58
research in recent years the human
32:01
genome and must of this is in recent
32:03
days the human genome the first draft of
32:06
the sequence was published in 2001 and
32:09
it's very clear the differences in our
32:12
genes are what this thing was you from
32:14
your neighbor and lead to diversity in
32:19
physical appearance and mental life
32:24
there are a number of ways people have
32:26
approached the genetics of autism as
32:29
kathy has said there's no question that
32:31
this is a genetic disorder and we must
32:34
undo
32:35
Stan the genetics that put people at
32:38
risk for autism I believe it's the best
32:41
way to understand environmental
32:43
influences is to understand the genes
32:46
that predispose to autism they may not
32:50
cause autism but they enhance the risk
32:53
for all sorts of environmental
32:56
influences and you've heard about many
32:58
of them in the lay press and in the
33:01
literature I think the best way to
33:04
understand truly what the environmental
33:06
risks are is to understand the genetic
33:08
risk factors now many people think of
33:11
genetics as having either an gene that's
33:15
functioning or one that is missing
33:18
perhaps because the the alphabet that
33:22
goes to make up the gene is wrong and
33:24
the genes code is misspelled and it no
33:28
longer makes a protein but it's now
33:31
become clear we really within the last
33:33
three or four years that it's not just a
33:37
yes or no issue one can have more or
33:42
less of the expression of a gene the
33:46
gene may be present but it may not be
33:49
speaking correctly to make proteins it
33:53
may be speaking too much so quantity is
33:56
important and gene expression is
33:59
critical and one approach is to look for
34:02
structural variations in the genome and
34:05
it turns out that ordinarily you inherit
34:08
one gene from your mother and one from
34:10
your father but since 2004 it's become
34:16
clear that some people have only one
34:19
copy of a certain gene some may have
34:21
three instead of the normal to some may
34:24
have four or five so quantity is
34:28
incredibly important and I show you this
34:31
slide simply to show you that the
34:33
technology is such that it is possible
34:36
to look through the whole genome in a
34:39
matter of a few minutes by cutting up
34:43
pieces of DNA
34:44
placing them as little spots microscopic
34:48
size spots on plates that are called
34:51
arrays and comparing one genome a
34:55
reference DNA with DNA from a test
34:59
subject let's say this is from a
35:02
participant in this study who has autism
35:04
and as you read along these gene are the
35:08
genome you can see just following the
35:10
blue line that in some cases the test
35:14
genome has a deletion or it may even
35:18
have a duplication and what has become
35:21
evident since 2007 I mentioning these
35:25
dates to tell you how recent these
35:28
advances have been that children with
35:31
autism have close to ten times as many
35:36
structural variations in their genome as
35:39
do control participants and the search
35:44
is on for what is in these segments of
35:47
deletions and duplications and how do
35:50
they affect the function of cells and
35:54
ultimately how do they affect the
35:56
behavior of children with autism let me
36:00
come back to our nerve cell one thing
36:02
that's very different about nerve cells
36:04
is that they form synapses they
36:09
communicate with other cells and impulse
36:12
once this cell adds up all of its inputs
36:16
from sensory information from activity
36:19
in the brain it send decides to send a
36:22
signal in the form of an electric
36:24
impulse out the the acts on the part of
36:29
the cell that communicates with other
36:31
cells now it's almost a truism but it's
36:35
a very it's an instructive way to think
36:37
of autism as a change in the timing of
36:41
these impulses there's something that's
36:44
not quite right and how these impulses
36:46
are orchestrated how they communicate
36:50
with the next cell in line and one real
36:52
possibility is that the defect may very
36:56
well be at these points of
36:58
or synapses that form between cells this
37:02
is a blown-up view of one of the
37:05
synapses when the impulse arrives right
37:09
at the end the nerve terminal is
37:14
signaled to release a chemical on to the
37:17
next cell in line it's called a
37:19
neurotransmitter and this transmitter
37:23
either excites the cell or it inhibits
37:25
it and it is critical to have the right
37:28
balance of excitation or inhibition to
37:33
in order to perform complex motor acts
37:35
sensory percepts and thoughts and
37:39
behaviors there is a gap between the
37:43
presynaptic the incoming cell and the
37:46
receiving cell and I want to talk about
37:48
that I'm going to give you a little bit
37:50
of detail to show you how rapidly the
37:54
genetics has advanced if I blow up this
37:57
segment the gap between the incoming
38:00
cell and the receiving cell it may look
38:03
like this the input releasing
38:06
transmitter and the postsynaptic
38:08
membrane receiving that transmitter and
38:13
I want to tell you a story at about a
38:15
black widow spider and the reason I've
38:18
included this is that it's my firm
38:20
belief but advances in autism will
38:23
really depend on advances in science in
38:27
many different areas so when we think of
38:30
supporting autism you must always think
38:34
of supporting research which is not
38:36
obviously related to autism it's the
38:39
whole enterprise which is critical this
38:42
story began with an interest in how of
38:45
venom from the black widow spider can
38:49
affect the communication between the
38:52
nerve terminal membrane and the membrane
38:55
on the receiving cell and indeed the
38:59
spider has a toxin that can be very
39:01
devastating to the synapse and within a
39:05
few years scientists in Texas and
39:08
England
39:08
and in other countries isolated this
39:12
venom and found out what molecules it
39:15
was affecting at the synapse this is a
39:19
drawing of the three dimensional
39:22
structure of these molecules this took
39:26
about a year after the discovery of the
39:28
molecules and they encode a family of
39:32
proteins called neuro directions in the
39:36
nerve terminal membrane and neuro
39:38
ligands in the postsynaptic cell
39:42
membrane these molecules are partners
39:44
they bind to each other and not only do
39:48
they cause these synapses to it here but
39:51
they seem to instruct the cell whether
39:54
to make an excitatory or an inhibitory
39:57
synapse now the interest from our view
40:03
this morning is that this is an insight
40:06
into how a synapse communicates and if
40:09
one believes as I do that autism is a
40:13
disorder in communication between cells
40:16
explaining the behaviors Kathy
40:18
Illustrated then we really have to learn
40:22
the whole cast of characters in the
40:25
incoming cell and the postsynaptic cell
40:28
none of these were now when I began in
40:32
science and when I studied synapses
40:34
throughout most of my career most of
40:37
these molecules shown here in this
40:39
cartoon have been discovered within the
40:42
last five to six years five to ten years
40:45
I would say but the striking thing is
40:48
the careful studies of families of those
40:52
copy number variants have pointed to
40:55
several molecules in the postsynaptic
40:58
and the presynaptic membrane that are
41:01
altered in children with autism so one
41:05
has the hope that we are on the right
41:08
track that if we understand more of
41:10
these alterations genetically we will
41:14
have a better handle on how they affect
41:17
synapses and community
41:19
pation and each one of these discoveries
41:22
offers the possibility of a new
41:25
therapeutic target to complement the
41:28
behavioral therapies that Kathy just
41:31
described now we won't be done there i
41:33
will i will tell you there's also hope
41:35
in the genetics maybe i'll end with us
41:39
to say once a gene is identified it can
41:42
be manipulated this is work of jay guy
41:47
and adrian bird in england where they
41:51
have identified a gene that leads to a
41:54
disorder that's similar to autism not
41:57
the same as autism and here they have
42:00
inserted the gene they have excuse me
42:06
they've removed the gene and without
42:08
going into detail it's possible to stop
42:11
the function of a gene by simply
42:14
inserting a stop signal in the genome
42:16
and when they did that the mouse they
42:19
they studied was obese and lethargic
42:29
this is a live movie in the mouse is
42:32
just not moving the striking thing is
42:38
this stop signal illustrating the power
42:42
of modern molecular genetics this stop
42:45
signal can be cut out and removed by
42:48
putting a chemical in the drinking water
42:50
so a jeans action can be stopped in this
42:54
case the stop signal and when they
42:57
looked at the mouse this is the same
42:58
mouse over here as we filmed as was
43:01
filmed here and when that mouse is
43:03
observed oops there it's thin it's
43:11
mobile and it's extremely promising to
43:15
me and hopeful that if a gene is
43:18
discovered hopeful for two counts is a
43:21
way to attack that gene and manipulate
43:24
it but also it says even here
43:28
a mouse that changes in the nervous
43:32
system are not permanent there is hope
43:34
in this type of experiment whether it's
43:36
in flies or worms or mice it suggests
43:41
that the plasticity of the brain is real
43:43
and that individuals can recover from
43:46
genetic and environmental factors now I
43:49
think because of the time I won't
43:51
continue but the next steps once we
43:54
discover genes is to find out where are
43:57
they working in the brain which circuits
44:01
in the brain are particularly vulnerable
44:02
and there's been great progress on that
44:05
front as well and but it perhaps in the
44:09
question-and-answer session we can
44:10
discuss that and then how those circuits
44:13
Walter behavior so we come to the table
44:17
with pull and matt and cathy i'm going
44:25
to start by asking questions and then i
44:27
think paul will come and leave a general
44:29
question and answer session Natalie I've
44:35
used a prototypic nerve cell but we know
44:38
that there are many many many different
44:41
kinds of nerve cells in the brain I know
44:44
that both you and pull are interested in
44:47
how you can study particular nerve cells
44:50
that might be involved in autism yeah I
44:53
would say the key question that we need
44:56
to address in animal models is which
44:58
circuits and cell types are affected in
45:00
these disorders and the way that you do
45:03
that is take genes that have been
45:06
implicated in humans make mouse models
45:09
like the one Jerry showed up there and
45:11
then ask in great detail out of the many
45:15
thousands of cell types that are present
45:17
in the brains in the brains of these
45:19
mice which ones are seriously impacted
45:21
by these genetic perturbations and Paul
45:24
and I over the last five years in our
45:26
laboratories and colleagues develop
45:29
novel methodology so that we can go
45:31
inside each one of those cells and tell
45:34
you exactly which proteins that comprise
45:38
the cell and which ones are altered in
45:41
any condition so this is a tremendous
45:44
advance because it not only gives us the
45:47
fundamental properties of the cell but
45:50
also tells us how those cells change in
45:53
let's say a mouse model of autism this
45:57
is the one way this is one way in which
45:59
you can ask ok and exactly what part of
46:02
the brain and exactly what cell and in
46:04
exactly what circuit are these have
46:07
animals abnormal and because we know
46:10
every protein made in that cell you can
46:14
also ask if these cells are abnormal
46:17
which proteins might we manipulate to
46:19
make them more normal so what we're
46:22
doing now is trying to use this
46:24
methodology to characterize the various
46:26
mouse models of autism and understand
46:29
the circuitry and the molecular
46:31
pathology in each of the cell types that
46:33
are relevant to the disease please
46:38
remember all this so you can ask
46:40
questions because it does bear
46:44
discussion and the only way to really
46:47
push these things as to ask is to ask
46:51
the questions no matter how focused you
46:55
think they are it's just tremendously
46:56
helpful to hearing your thoughts well
46:58
you've been interested in therapeutics
47:00
your whole career how would you approach
47:03
there are no good I think really
47:06
specific medicines independent of
47:09
behavioral therapy for autism but I know
47:11
you've been thinking about this and you
47:13
know how would you approach this the way
47:17
that men are approaching this on our
47:21
labs and by the way one of the most
47:24
important people in this is a young lady
47:26
in the third row Miriam Haman who I
47:28
would ask to stand up but she's very shy
47:30
and she'll be angry with me if I forced
47:33
her to do that I know there's she over
47:35
five years develop this extraordinarily
47:37
powerful technique so that is now as
47:41
matt said possible to look at all of the
47:44
proteins in any given individual nerve
47:46
cell type and try to understand in mouse
47:48
models of autism and the same concepts
47:52
can be applied to other
47:54
neurological and psychiatric disorders
47:56
to understand which cell types are
47:58
involved and which proteins in those
48:00
cells are involved the limitations right
48:03
now are the fact that whether to fold
48:07
let me tell you what the concept with
48:09
our concept was we would take these
48:12
mouse models of autism and then find out
48:16
what's wrong in those models and that's
48:19
what we're trying to do the one
48:22
difficulty there is that it's very hard
48:24
to get mouse mice to do the very
48:26
complicated behavioral things you saw
48:28
Cathy Lord show you it's impossible
48:32
basically so we have to hope that these
48:35
genetic changes that go on in the human
48:37
are in the initial steps very similar
48:40
ones that go on in the mouse and it is
48:42
faith in that possibility that arises
48:45
program another tool that we have
48:47
available is these the various
48:51
medications that have partial ability to
48:55
treat autism perhaps Kathy would like to
48:58
talk more about that but some of them
49:01
are effective with certain aspects of of
49:04
autism and others are not but we're
49:07
hoping using those same drugs that had
49:10
some i'll be at limited clinical
49:12
efficacy to study what happens in the
49:15
behave in the biochemistry of the mouse
49:17
models I'll throw something out there
49:24
and then if it just duds you can move on
49:26
but what like watching your little obese
49:29
Mouse who wasn't moving my first
49:31
reaction is if that was a child we would
49:34
be trying to figure out like why isn't
49:37
it and and what could we do to get it to
49:41
move and why is it obese and I mean and
49:43
in what are the factor how did it get
49:46
there so that's one question and then
49:49
how do we change that behavior partly
49:52
because kids with autism are here and we
49:55
can't just wait you know we can't wait
49:58
for the neuroscience while they're here
50:01
to figure out what to do but it but it
50:03
also struck me even as you are saying
50:05
you can't we can't do a baby a das with
50:07
a mouse and it wouldn't mean anything
50:09
but there's still a question isn't is
50:12
the mouse development so fast that you
50:16
can't look at how you get to a point
50:18
where you have something that you're
50:22
trying to account for does that mean yes
50:24
it does I mean Lee and many people will
50:28
question the use of my sand flies and
50:33
worms with with good reason but in some
50:35
cases but this is a case where a mouse
50:39
is not a human and you have to accept
50:40
what the mouse exhibits so while this is
50:43
not exhibiting social withdrawal or lack
50:48
of social communication we know this
50:52
gene is involved in a human disorder so
50:55
the animal was obese and a mobile that
50:58
points to a certain region of the brain
51:00
called the hypothalamus which is known
51:05
to regulate feeding behavior and weight
51:07
control and so but the hypothalamus has
51:12
many other functions including social
51:15
interaction functions and emotional tone
51:18
so it points to the hypothalamus and I
51:21
think this very important study has
51:24
attracted the interest of scientists to
51:26
go back to the hypothalamus perhaps
51:29
using and I think one of the
51:30
investigators that who does aadmi is
51:33
using your ribosome capture technology
51:38
to study genes in the hypothalamus
51:40
hoping to go from human to mouse and
51:43
then back to human so I think the
51:45
behavior is relevant I think this
51:48
reversibility of the phenotype of the
51:51
mouse that Jerry showed you is very
51:52
important because that's an instance
51:55
where you've provided the normal
51:58
function of the protein back in an adult
52:00
and in reverse the developmental
52:02
phenotypes so that's a stunning example
52:05
that if you can somehow intervene it's
52:09
not a permanent disorder the second
52:11
concept that everybody should take away
52:13
from this is that if we are able to
52:15
identify
52:16
the circuits that are involved in autism
52:19
spectrum disorders and I think we will
52:22
be through all of this intensive
52:24
research there are ways to treat search
52:26
circuits and improve their function that
52:29
don't necessarily require that we
52:31
reverse the initial pathologic event so
52:35
we can treat a piece of a circuit to
52:37
increase its activity or decrease its
52:39
activity to compensate for the
52:41
abnormality that's present this concept
52:45
is very important because in order to do
52:47
that we need to know what targets what
52:49
sells in once circuits we're going to
52:51
treat whole do you want to take some
52:58
question
53:00
I think we're close to time to opening
53:03
it up for questions from the audience I
53:05
think we're hearing that this disorder
53:08
is really an area that will profit from
53:13
study in a very wide range of
53:16
disciplines and models from observation
53:20
of children right down to molecular
53:23
genetics in mice and they all have their
53:25
contribution to make well I want to open
53:28
it up this discussion to questions from
53:30
the audience would you repeat the
53:32
question a question was could we comment
53:35
about vaccines and white noise as they
53:38
pertain to autism I know more about
53:41
vaccines than white noise but I think
53:44
that that there is no evidence that
53:47
vaccines cause autism at we can never
53:53
say and that for an individual child
53:56
that vaccines didn't contribute to
53:59
autism and we need to be careful because
54:00
they're there certainly could be a case
54:03
or cases where this figured in autism
54:07
but the two main reasons why people have
54:11
become concerned about the contribution
54:12
of vaccines to autism has been the
54:15
growing prevalence of autism thinking
54:19
that you know autism is increasing at
54:21
the time that we are having different
54:23
vaccines and babies are getting more
54:25
vaccines but i think it's become clear
54:30
that even when we take the components of
54:32
vaccines out which people had proposed
54:35
were contributing to autism and when the
54:37
particular vaccines I mean it's shifted
54:39
the argument of which vaccines and when
54:41
has changed numerous times in the last
54:44
20 years when those things change that
54:47
the prevalence of autism is continuing
54:50
to it grow certainly to some degree
54:53
because of changes in definition and
54:56
increasing awareness and then we don't
54:58
know but whatever it is it does not
55:00
follow the pattern of vaccines the
55:02
second source of concern about vaccines
55:06
came from work by Andrew Wakefield that
55:09
looked at an association between the MMR
55:12
vaccine and gastrointestinal
55:14
an autism that work has now been
55:16
repudiated on numerous levels numerous
55:20
times and so it's clear that that that
55:23
link is not there so I think where we
55:26
are left is it's very hard to prove the
55:28
null hypothesis to prove that vaccines
55:30
never caused autism and I think but I
55:34
think what we can say is that vaccines
55:37
prevent disease that can have very
55:41
serious effects and that is known and
55:44
there is no known link between vaccines
55:47
and autism now i know many parents
55:50
remain concern because there is a
55:53
phenomenon in autism which involves
55:55
losing skills or regression that does
55:57
occur at about the same time that
55:59
vaccines are given and this the
56:02
phenomenon of regression is very we
56:04
don't know what it means and it's very
56:06
hard to understand and it and it is very
56:09
heartbreaking for anybody who's ever
56:12
seen it and I think that link between
56:14
time and and vaccinations has has meant
56:18
that it's almost impossible to take away
56:21
the fear that families have but there
56:23
there is no controversy really that
56:26
vaccines are do not account for the
56:30
majority of cases of autism or even a
56:33
substantial minority white noise I've
56:36
just probably read you know things in
56:38
the media so so basically i don't i
56:42
don't know i should probably just stay
56:44
out of that one anybody else want to
56:45
comment on white noise i bet there any
56:49
comments from the rest of the panel
56:50
where any more comments from the rest of
56:54
the panel wonder where they kathy my
56:56
expected and why despite many studies
56:59
that have failed to provide evidence in
57:01
support of the vaccines hypothesis or
57:03
what isn't why this keeps on and on and
57:05
on it we took people won't let it die
57:08
it's a very it's a very powerful image
57:12
you know if a child at a certain age
57:15
receives many vaccines in a very short
57:18
period of time
57:19
and then apparently and I think this is
57:21
quite controversial apparently regreses
57:24
although on close observation many of
57:27
these children are exhibiting some signs
57:30
of the subtle ones Kathy pointed out
57:33
even before the vaccines but you know
57:36
the public does is not easily convinced
57:40
by probabilities then it's very hard
57:43
it's an issue i think in how we
57:45
communicate about science and a public
57:49
understanding of science I think the I
57:54
think the argument will keep coming back
57:56
and the concern coming back until we
57:58
understand more about molecular
58:00
mechanisms and the genetics of autism
58:03
there are people interested in immune
58:08
responses and immunology and once we
58:10
understand that I think then we'll have
58:13
a more direct test of the vaccine
58:15
hypothesis but I quite agree with Kathy
58:18
the overwhelming epidemiologic evidence
58:21
is negative there's no correlation with
58:26
vaccines and autism good so we I hope
58:29
the microphones now working who has it
58:30
yes thank you um I'm curious about the
58:34
treatment the potential treatment using
58:36
your obese Mouse study it's a two-part
58:40
question is the chemical stop that you
58:44
would use to reverse the phenotype is
58:47
that irreversible and or how long does
58:51
it last for just briefly i'll be glad to
58:53
talk to you about it later the
58:56
experiment i showed was was artificial
58:59
in the sense that a critical gene had
59:03
been identified and the investigator in
59:05
that study used a molecular trick to
59:09
turn off the gene as the animal
59:11
developed that's not that's not a
59:14
therapeutic it's it's an experimental
59:16
manipulation to turn off the gene and
59:19
then so there was something artificial
59:21
placed in the chromosome and then he was
59:24
able to remove that break on the gene
59:27
action so he demonstrated that when he
59:30
removed the
59:31
the gene could function again and the
59:34
animal recover but that's not a direct
59:36
route to a medicine but it points to the
59:40
possibility of a medicine I think that's
59:42
I think it's important to underline the
59:46
fact that that kind of experiment which
59:49
gave us a fundamental insight into
59:51
reversing the phenotype of these mice
59:53
can't be done in any species of mammal
59:56
except for mice so the genetic tools
60:00
that we have available to investigate
60:02
these diseases in this small animal are
60:05
actually critical for us to get game
60:07
fundamental insights into the disease we
60:10
couldn't do that experiment in a higher
60:13
mammal and the gene actually also wasn't
60:16
a gene for autism the gene was a gene
60:18
for rett syndrome so it's I think the
60:22
jury's point was this is a model for
60:24
what we hope to get to in terms of
60:29
eventual treatment the idea that this
60:31
may be able to work but it's not that
60:34
there's an autism gene that you can turn
60:35
off that makes mice that have autism
60:38
stop being autistic yeah so now I think
60:42
a question just here in the middle I'll
60:44
come to the front in a moment dr. fish
60:47
back you've mentioned environmental
60:49
factors as well but didn't go any
60:52
further so if you have a gene that's not
60:54
functioning that's impaired or the cells
60:57
aren't functioning properly and then
60:58
environmental factors such as toxins are
61:01
you know ingested and two small children
61:04
does this have an effect on their their
61:09
development and could this autism
61:11
spectrum develop at this time I've ever
61:14
read so many articles on children that
61:16
have a reduction of toxins and all of a
61:19
sudden they're seen to have a huge
61:21
improvement you just didn't really go
61:24
any further with the environmental
61:25
factors it's a complex phenomenon I
61:31
think there are many things that can
61:34
modify the action of genes and that's
61:37
what I think offers so much hope that
61:40
there are genes that increase the risk
61:42
and there are modifier genes that might
61:45
actually decrease the risk so it's not
61:48
going to be I think what kathy was
61:50
getting at one gene one disorder I think
61:54
there's we're going to have to deal with
61:56
a mathematical approach to understanding
61:59
how these genes interact and what the
62:02
final cellular result is what the final
62:06
circuit result is and then hopefully
62:08
what the final behavioral result is as
62:11
we move up the ladder so I'm I don't
62:14
know of any modifiers yet but I think we
62:18
can't rule those out right could we in
62:22
the front the gentleman in the front
62:24
could you wait for the microphone is
62:26
just coming so one comment was one of
62:30
the debates is whether this is a
62:31
systemic disease or is really limited to
62:33
the neurologic system the CNB difference
62:36
between autism children and not is that
62:41
limited to a subset of genes or family
62:43
of jeans or is a genome-wide the second
62:46
question which is for or comment for dr.
62:48
Heinz's there are some clinical clues as
62:51
to therapies that at least when you look
62:53
at large registries of data or more
62:55
helpful than others and those might as
62:57
you start identify proteins and families
62:59
of proteins involved give you some some
63:01
greater in size to therapeutic
63:03
approaches so I'll be brief on the first
63:06
one remember the study I cider was 2007
63:10
many people are asking are these copy
63:14
number variants recurrent how common are
63:17
they do they are we seeing them over the
63:20
same ones over and over again the answer
63:23
is there may be fifty to a hundred of
63:25
them
63:26
and they may occur in one to two percent
63:28
of the population at risk but we're just
63:32
now and the Simons Foundation is
63:35
involved in a very large study to see
63:37
are there hot spots in the genome where
63:41
there are certain variants which are
63:43
really much more likely to recur we
63:46
don't know that yet good what was the
63:52
second any more comment not do you want
63:54
to comment further the second part of
63:56
the question was about therapies and I
63:58
think Paul outline this but because we
64:02
can look at the molecular events that
64:04
occur in any cell type in response to
64:06
let's say a genetic perturbation we can
64:09
look also at these events in response to
64:12
any therapy so any therapy that is
64:14
either that is relevant and important
64:17
for our treating autism that's developed
64:20
we can assess in mice and try to figure
64:22
out what circuits it's actually
64:25
impacting this is critical if we're
64:27
going to develop new therapies I think
64:31
there was a question in the front yes
64:33
what is the relationship between a what
64:38
is the relationship between the gastro
64:41
internal problems in autistic children
64:43
as well as behavioral problems and
64:45
autistic children and the toxicity of
64:46
what they eat like unprocessed foods
64:49
processed food excuse me
64:53
we don't know I mean I mean there's
64:58
there's there's certainly reason to
65:01
believe that if you have
65:02
gastrointestinal problems that is going
65:04
to affect your behavior so I think I
65:06
think we need to remember that anybody
65:08
who is uncomfortable or in pain is going
65:11
to act differently and I don't think we
65:13
should negate that I mean I'll say
65:15
quickly of I have there's a 20 year old
65:18
young man that I've known forever who is
65:20
here in New York who I just saw and his
65:23
father told me last weekend he said to
65:25
the boy or young man said to his dad dad
65:29
my heart's on flame and he pulled his
65:32
shirt up and said can you blow on my
65:35
heart and make the flame go down and
65:37
then he said that's you know his name or
65:40
say johnny johnny has sad heart johnny
65:44
wants a happy heart and i think i think
65:47
he probably had heartburn is i mean i
65:50
don't i don't know and i don't think
65:52
anyone knows but i think he was trying
65:54
to say that he had some kind of
65:57
indigestion but out but you know he
66:00
can't talk about that and so I think
66:02
that does contribute to this is a boy
66:05
who can be very aggressive when he's
66:07
unhappy and and we've been trying to
66:10
figure out why has he been so aggressive
66:12
recently so I think that link just you
66:15
know just the same length that it would
66:17
have for anybody is something we can't
66:19
discount in addition you know I think
66:21
that there have been hypotheses about
66:23
more complex links between GI function
66:27
and brain function which so far have not
66:29
stood up on any end as far as like I can
66:33
tell those are not over did you know I
66:35
want to be emphasize a point that the
66:38
the brain is not sitting up here in
66:41
isolation from the rest of the body
66:43
indeed we have nerves throughout every
66:47
organ in the body especially the bowel
66:49
and weary and the brain receives inputs
66:52
and a very real sense our sense of self
66:56
is is is in large part determined by
67:00
impulses that arrived from different
67:03
organs in the body
67:04
do you are you feeling pain are you as
67:08
your stomach upset all these things
67:11
offer a certain continuity to the self
67:13
so I am I especially am interested in
67:16
what are called these autonomic uh most
67:19
unconscious inputs from the body to the
67:23
brain and there's a great deal of
67:24
interest now in neuroscience to
67:27
understand how these inputs eventually
67:30
influence behavior and conscious
67:33
behavior where the union is between
67:35
these unconscious inter effective some
67:39
people call them inputs and conscious
67:42
behavior and I think it's a very
67:44
understudied phenomenon there certainly
67:46
are genes in common between the bowel
67:49
and the brain and many children come to
67:54
the doctors the food this was always my
67:57
night miracle that I would be cool while
68:03
I was saying something brilliant they're
68:08
endangered happen between the brain in
68:11
the bell and and um so we have to be
68:15
aware of all the time but i agree with
68:17
kathy that there's no obvious clinical
68:20
connection yet and how it gets back to
68:22
unprocessed food we don't know but i
68:24
think we probably all wonder pole one
68:29
important aspect of what is it an
68:31
autistic a research that we've not
68:34
really emphasized today and we should
68:35
have has to do with the heterogeneity of
68:38
the disease it was implied in the slides
68:40
and kathy showed on autism spectrum
68:43
disorder but it's actually a whole bunch
68:46
of different diseases and this is
68:48
somewhat slow down progress in fact this
68:51
program that Jerry talked about that the
68:54
Simons Foundation is carrying out
68:57
involves looking at these different
68:59
subclasses of autism and trying to get
69:01
the genetic basis for each of these as
69:03
separate disease entities and once that
69:05
information is generated and from what
69:08
he told me yesterday this will be in the
69:10
next year or two we'll have a pretty
69:12
complete story of the genetic basis for
69:14
each of these subclasses of autism
69:17
we then a lot more rapid progress being
69:19
made in the laboratory and trying to
69:21
understand the molecular consequences of
69:24
these genetic mutations in the
69:26
individual types of participant an
69:28
article appeared just one edition in the
69:31
New England Journal of Medicine last
69:33
year saying the children with autism
69:36
seem to improve when they have a fever
69:40
and this is another example and Marilyn
69:44
and Jim have told me repeatedly from
69:45
from personal experience that this seems
69:49
to be the case and again it's an example
69:51
of these unconscious functions of the
69:54
hypothalamus and fever and we must learn
69:57
what those connections are in the middle
70:01
yeah hi um I think the reason why the
70:07
vaccine issue will keep coming up and
70:10
many of the questions you're receiving
70:13
will keep hounding the scientific
70:15
community is because all parents of
70:17
children anywhere on this spectrum want
70:21
to be partners in resolving this issue
70:23
while we wait for science to catch up to
70:26
the need and so my question is for dr.
70:29
Lord as a parent walks in with a very
70:32
young child and his first thrown into
70:35
this world of a child they can't relate
70:38
to or control or soothe what do you what
70:42
how do you impart if any wisdom to the
70:45
parent to comfort them so that they can
70:47
be a partner at home is there a general
70:52
dietary suggestion to vary the diet to
70:57
limit certain foods or two soothing
71:00
music are there any general therapeutic
71:04
recommendations that you make to a very
71:06
lost parent I think that our focus is
71:13
very much on behavior I mean trying to
71:15
see what it is that the child can do
71:17
because kids can you know all kids can
71:20
do some things I'm trying to see what
71:23
our kids interested in and then trying
71:26
to see what is holding them back and
71:28
then trying to piece together
71:30
they're those aspects of behavior so
71:33
that the world makes more sense to the
71:35
child so that the child can communicate
71:37
the things that they're thinking but
71:39
then also to pull that child into our
71:42
world as much as we can in a pleasant
71:46
way I think we also want parents to be
71:49
parents and I think what's what's hard
71:52
is that I think parents of children with
71:55
autism are immediately tossed into a
71:57
world where they have to be protectors
72:00
advocates business managers you know
72:05
scientific you know wardens in some ways
72:10
and and I think trying to be able to say
72:13
all right what does this what can we do
72:15
with your child now and where is this
72:17
going not in 20 years but for tomorrow
72:20
what do we want your child to be able to
72:23
learn and then let's look at the good
72:25
things or child can do and take those
72:27
strengths and try to use those to build
72:32
up the things that are hard also not
72:34
forget the strengths because in the end
72:35
those strings are going to make it as
72:37
much of a difference as the hard thing
72:39
so I think we don't put people on diets
72:42
I mean many families that we see do have
72:45
kick it said kids on diets and I think
72:47
certainly being sensible about what your
72:49
child eats is true for any parent but I
72:54
think that we don't think there's a
72:55
single key there's just you know taking
72:59
it one step at a time that's hard though
73:02
because it's a pretty overwhelming
73:04
experience and many of you can testify
73:06
about that far far more than I can but I
73:09
think also remembering their kids you
73:12
know and their kid you know there are
73:14
all kinds of things about being kids
73:15
things you like things you don't like
73:17
things you can't do things you won't do
73:19
and how do we work around that and not
73:22
forget ultimately this is a person you
73:25
know they're here and and in a family
73:28
and not let that get you know tossed by
73:31
the wayside I think we still have a
73:35
couple more questions over here at the
73:37
very well there's two there so one there
73:39
and then one at the back
73:41
a question why do we see this more often
73:47
in boys than girls if we could answer
73:51
that question you want to answer the key
73:54
question and you know the what many
73:56
people would say right away is that it
73:59
has something to do with the X
74:00
chromosome but the best data to date are
74:03
that that's not true so again it's these
74:06
modifying factors there's something
74:09
about the women and the dimorphism and
74:13
women are not identical with men
74:17
something about the dimorphism in the
74:19
body and the brain that might be
74:21
protective is one hypothesis hi thank
74:27
you as the mother of an 11 year old
74:29
Asperger's son I'm curious dr. Lord you
74:33
were talking you had a young man at the
74:35
on your video and you you had a social
74:39
group or something I found in my
74:42
experience that I have tried every
74:45
traditional psychotherapy cbt sort of to
74:50
enhance his social ability and it I was
74:55
struck by my suspicion is that your
74:59
group was for observation purposes or
75:01
have you or have you found benefit
75:03
through a social skills group and things
75:07
like that we have found some benefit
75:09
with medication we run groups that mean
75:17
we call social groups there I think that
75:20
partly we feel they work but partly our
75:23
expectations are quite different than a
75:25
social skills group I mean these groups
75:27
run forever I mean the kids now I mean
75:30
they're now a hierarchy so we have eight
75:32
of them in Michigan and like the teens
75:34
all want to move into the older teens
75:36
group and the older teens into the
75:37
adults people do move out of them I mean
75:40
if they get a social life that is that
75:42
you know they have something better to
75:43
do but I think what we our first line of
75:47
our first goal is shared enjoyment we
75:50
want it to be positive we want the kids
75:52
to interact
75:52
each other we also include typical peers
75:55
and then the idea is not to teach us
75:58
skill but for each participant in the
76:01
group these are these are clinical
76:03
groups we have goals for that child so
76:06
that's this the boy that you saw but is
76:08
very interested in interacting he has
76:11
all kinds of approaches the problem is
76:13
not that he doesn't want to be around
76:14
people it said he doesn't know quite
76:16
what to do and he's the kind of kid
76:18
who'd go right up to the nose of the
76:19
person that he likes and talk in their
76:22
face and so a goal is let's back off I
76:25
mean for him and another child the goal
76:29
may be getting them into the group so we
76:31
have very pragmatic goals we just
76:33
readjust those goals about every three
76:35
months with the parents and other
76:37
teachers and then in the groups which
76:39
meet for about an hour and a half once a
76:41
week we try to create positive
76:44
activities that really pull the kids
76:47
into social interaction I think our
76:49
hypothesis is that many almost all kids
76:53
with autism and adults don't have enough
76:56
opportunities to interact with other
76:58
people because other people don't stay
76:59
with them long enough but if you do stay
77:02
with them people like them and they like
77:04
other people so we're trying to create
77:07
that and you know my fantasy is that
77:10
this you know this will move on I mean
77:13
we did have for example a group three
77:15
men in the adult group just rented an
77:18
apartment next door to our clinic much
77:20
to our surprise but they did it I know
77:23
on their own so that's where we're
77:25
trying to go and we have some data where
77:28
we follow this where what we show is
77:31
changes not so much in high level skills
77:34
immediately but long-term changes in the
77:37
positive attitude toward people
77:39
assumption that someone will like you if
77:42
you tolerate them decreases in
77:44
inappropriate behavior and then just
77:47
changes for example in proximity when
77:49
you walk into a room in the group how
77:51
long does it take you to get me
77:53
interacting with someone else that kind
77:55
of thing so we're not claiming we're
77:58
curing anything but it does feel like
78:00
relationships are really developing
78:03
and that's what we want to do we feel
78:05
like if we can set the stage for that to
78:07
happen and then provide guidance sort of
78:11
in the background then then good things
78:13
will happen that again are just one drop
78:16
in the bucket so there are many other
78:18
approaches that need to go on at the
78:20
same time I'm afraid I'm going to have
78:22
to stop the questions there because
78:25
we're over running thank you very much
78:28
to our speakers thank you for our
78:29
panelists thank you
78:41
you73726
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