NEUROBIOLOGY OF BRAIN DEVELOPMENT FROM CHILDHOOD TO ADULT

Episode Transcript

Speaker 1 (00:01):
Well come Today, we're going to be looking at biological
foundations of human development. So brain development begins prenatally and
follows the trajectory shape by critical periods synaptic pruning and myelination,
prefunnal cortex matures, last explaining a lot of the risk
taking and impulsivity that we see in adolescence. And the

(00:24):
last part that really hasn't matured is usually the white matter,
the myolination. Early experiences shape what they call the neural
architecture through use dependent plasticity. We'll talk about that. How
the brain develops in the different stages. Teratogen's malnutrition and
early stress can disrupt brain circuits and lead to long

(00:46):
term developmental and psychological impairments. Autism spectrum the sre in
ADHD reflect altered brain activity, timing of development, and neurotransmitter function.
The brain itself builds it in stages, starting even before
birth in uteros when it actually begins, so the foundation

(01:12):
is late early if you're looking at it. The remodeling
continues well into adulthood. One of the things you'll be
tested on is the timing, sequence and conditions of brain development,
shape behavior and highly shape behavior. Cognition, and vulnerability to others.
So we'll look at some of those things today. Well,

(01:41):
let's look at early childhood development. We're going to start
with prenatal brain development just weeks after conception, which is
a highly sensitive time to disruption. It includes the following phases. Neurogenesis,
the birth of neurons, mostly completed by mid gestation. Neuronal migration.
Neurons move to correct locations in the brain, differentiation, neurons

(02:05):
specialize into motor, sensory or inter neurons, and then synaptogenesis
formation of synapses begins latent gestation and explodes after birth.
You have to be able to order these steps and
identify which ones are sensitive to teratogens. Our most vulnerable
times are second the second trimester of the pregnancy. That's

(02:30):
when a lot of the brain development happens, especially what
they call the hormonal flush. Also recognize that the neural
tubes formed very early and it's the precursor to the
brain and spinal cord. So a lot of these earlier
teratogenic effects can affect development of movement and other factors
in the spinal corkers that hasn't developed in that second trimester.

(02:53):
The fourth of the six months. You have a lot
of issues there. Teratogens substance that disrupt fetal development and
cause lasting brain abnormalities, something that is not on the
example of interest. They have tested the placentas of males
and females and found that the males tend to be
a little bit more vulnerable to teratogenic effects, making them

(03:16):
more susceptible to delaying of maturation of brain development over
the course of time. Some of the teratogens include drugs, marijuana, cocaine.
Also alcohol. You can think about fetal alcohol syndrome which
impairs neural migration, having neurons moving from one place to another, microcephaly,

(03:38):
the shrinking of the brain or the skull. Poor impulse control,
which as we know as in the executive function area
and the prefunnal cortex leads another one that disrupts synaptic
growth and lowers IQ and increases risk of attention problems.
Again in that prefunnel cortex area, maternal stress elevates cortisol,

(03:59):
disrupts h PA access and affects fuel brain connectivity, so
the HPA access to the stress system supporting to other
timing and dosage of a triatogen exposure, which determines its
effect early gestational exposures global brain late exposures localized impairments.
If we go to early childhood brain development by h

(04:20):
five of the brain is ninety percent of its adult size,
but its connectivity, not size, determines function synaptic overproduction and pruning.
Initially more connections of form than needed than through pruning,
unused synapses are eliminated use it or lose it principle. Here,
a lack of stimulation can result in excess pruning and

(04:41):
reduce neural networks, something we saw with institutionalization. Myelination again
is the fatty cloating or fatty fatty coating of axons
that speeds up neural transmission. It's like a freeway. The
myelination occurs in sensory motor regions first and continues into
the pre cortex into the mid twenties, affecting impulse control

(05:03):
and planning. See in adolescence, most of the brain structure already
fully developed, which lacking is the connectivity. Highways aren't fully there.
So all the streets are already developed, but that city
doesn't have is the freeways fully developed Till your mid twenties.
They estimate twenty four to twenty five. For the exam,
you need to know the association in executive areas the

(05:23):
mile and eight later. The deficits here are linked to ADHD,
trauma and stress. So if you have terretogenic effects, this
can delay the maturation of the prefunnel cortex area and
the myelination sensitive periods and attachment. The brain's most responsive
to positive or negative environmental input during early sensitive periods,

(05:46):
so negative experience with abuse neglect equal Thinner cortexes reduce
great matters for processings compromised a hyperactive amigala, so hypervigilance
is going to be detective here. They're going to see
threats where there are none positive so is the opposite.
So when you have secure attachment strengthens the brain architecture
and have a much healthier outlook for the exam no

(06:08):
secure attachment and response caregiving and how they serve as
protective factors against later psychopathology. Adolescence is marked by mismatch
in brain maturation. The limbic system, rewarding emotions develop early
prefunnel cortex judgment regulation matures into the mid twenties. This
explains why risk taking happens pure influenced sensitivity, mood oder emergence,

(06:30):
mood disorder, emergence, and impulsivity. Again, a lot of these
areas are in the pre funnel cortex. As you mentioned,
one thing you'll need to know nor that the reward system,
the nucleo ciccumbents is highly active during adolescence. Teams are
more reactive to novelty and immedia gratification. Again because the
prefhoidal cortex highway isn't fully developed, so the emotions by
the time they get to the pre formed to cortex

(06:52):
to get a process, it's very slow biological and also
you got to remember every adolescent it's different to the
degree of this. That's why some adolescents may not be
as impulsive as others or as risk takers as others.
So it's going to be parenting the development better stronger
development of their prefunnel cortex. There's a lot of factors here,

(07:13):
the biological impacts of early stress and mountnutrition, HPA, access
dysregulations of cortisol, overproduction, hippocampal damage, impaired feedback loops. Symptoms
would include anxiety, effective instability, and memory problems AMIGDA overactivation
heightens threat detection and emotional reactivity seen in PTSD, anxiety

(07:36):
disorders and early trauma survivors, and once again, prefunnel cortex
under development linked to poor at tension, impulse control and
executive function, slower myelination and synapsformation due to poor nutrition
or chronic stress. For you to pay attention to is
know the timing is everything. Earlier exposures lead to more
severe impairments neuer development to disorders, autism, spectrum disorder, core symptoms,

(08:02):
social communication deficits, restrictive competitive behaviors. Neurological features include atypical connectivity,
over connectivity in some areas, under connectivity in others, early
brain overgrowth and frontal and temporal lobes, impaired mirror neuron systems,
and genetic careriatabilities about eighty percent, So be ready to

(08:22):
identify structural and functional brain differences in the amigala insulin
mirror neuron deficits. No the role of early intervention remapping
these circuits for the e triple p ADHD core problem.
Delayed maturation of prefunnel cortex affecting attention and impulse control.
You can see it overlaps quite a bit with autism,
and we're seeing a lot of this comorbidity diagnosising. Now

(08:44):
these codiagnosises, neurobiological findings activity and dorsal lateral prefunnel cortex,
anterior singular, basal ganglia, cortical thickness, peak and activation and
executive control networks. Pharmacological interventions stimulants which improve member dopamine
and epidephrine transmission, also PFC activation combined with behavioral strategies

(09:07):
that actually works much better being able to match the
brain regions as functions, but symptoms are going to be
good for the E triple P expect questions on how
stimulants normalize under developed circuits in which neurotransmitters are involved.
Don't forget the dopamine and nouro epinephrine for ADHD, as
well as dorsal lateral prefunnel cortex, anterior cingulate, and the

(09:29):
basal ganglia. So that starts covering a little bit of
our biological for the development of the individual. Some other
things I wanted to look at. We talked earlier about

(09:49):
the reward center for the children or for adolescens. It's
the nucleus incumbents is what you need to know is
particularly active in adolescence. This makes teams highly responsive to
novelty and immediate rewards, sometimes at the cost of long
term consequence, and so prefundal cortex is also associated with

(10:10):
anticipatory function, so anticipating what could happen, and the MRI's
adolescents reward circuits light up faster and more intensely than
control networks, which is no surprise. The prefundal cortec doesn't
fully catch up until the mid twenties, which is that
which has implications for treatments, legal policy, and education. So

(10:31):
it's important to know that when we look around, let's
see if there's anything else I've missed well, from fetal
brainstem formation to adolescent prefrontal pernium, the trajectory of brain
development is anything but linear. Just remember its shaped like timing,
experience and interaction between biology and environment. So make sure

(10:52):
you understand that. And that's it for today. We're going
to be talking about tomorrow or next week. Actually we'll
take this week this weekend off. Psychoeurominology and the biology
of stress is our next ones. We'll be looking at
the immune system and how it associates with psychology and
the nervous system. It won't be recording on the weekends.

(11:13):
So what you can do is go back and revisit
this week's lectures, and as the weeks go on, you
can revisit from the beginning, so you have plenty of material.
Hopefully the months go forward. We should be doing this
probably for three or four months, and then if people want,
we'll go into advanced stuff into these areas and maybe
that'll help you better understand some of the concepts. If

(11:36):
you're don't