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NEUROBIOLOGY OF BRAIN DEVELOPMENT FROM CHILDHOOD TO ADULT · Understanding the Brain

• 0:01
  Speaker 1: Well come Today, we're going to be looking at biological
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  Speaker 1: foundations of human development. So brain development begins prenatally and
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  Speaker 1: follows the trajectory shape by critical periods synaptic pruning and myelination,
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  Speaker 1: prefunnal cortex matures, last explaining a lot of the risk
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  Speaker 1: taking and impulsivity that we see in adolescence. And the
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  Speaker 1: last part that really hasn't matured is usually the white matter,
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  Speaker 1: the myolination. Early experiences shape what they call the neural
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  Speaker 1: architecture through use dependent plasticity. We'll talk about that. How
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  Speaker 1: the brain develops in the different stages. Teratogen's malnutrition and
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  Speaker 1: early stress can disrupt brain circuits and lead to long
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  Speaker 1: term developmental and psychological impairments. Autism spectrum the sre in
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  Speaker 1: ADHD reflect altered brain activity, timing of development, and neurotransmitter function.
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  Speaker 1: The brain itself builds it in stages, starting even before
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  Speaker 1: birth in uteros when it actually begins, so the foundation
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  Speaker 1: is late early if you're looking at it. The remodeling
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  Speaker 1: continues well into adulthood. One of the things you'll be
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  Speaker 1: tested on is the timing, sequence and conditions of brain development,
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  Speaker 1: shape behavior and highly shape behavior. Cognition, and vulnerability to others.
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  Speaker 1: So we'll look at some of those things today. Well,
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  Speaker 1: let's look at early childhood development. We're going to start
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  Speaker 1: with prenatal brain development just weeks after conception, which is
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  Speaker 1: a highly sensitive time to disruption. It includes the following phases. Neurogenesis,
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  Speaker 1: the birth of neurons, mostly completed by mid gestation. Neuronal migration.
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  Speaker 1: Neurons move to correct locations in the brain, differentiation, neurons
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  Speaker 1: specialize into motor, sensory or inter neurons, and then synaptogenesis
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  Speaker 1: formation of synapses begins latent gestation and explodes after birth.
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  Speaker 1: You have to be able to order these steps and
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  Speaker 1: identify which ones are sensitive to teratogens. Our most vulnerable
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  Speaker 1: times are second the second trimester of the pregnancy. That's
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  Speaker 1: when a lot of the brain development happens, especially what
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  Speaker 1: they call the hormonal flush. Also recognize that the neural
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  Speaker 1: tubes formed very early and it's the precursor to the
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  Speaker 1: brain and spinal cord. So a lot of these earlier
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  Speaker 1: teratogenic effects can affect development of movement and other factors
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  Speaker 1: in the spinal corkers that hasn't developed in that second trimester.
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  Speaker 1: The fourth of the six months. You have a lot
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  Speaker 1: of issues there. Teratogens substance that disrupt fetal development and
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  Speaker 1: cause lasting brain abnormalities, something that is not on the
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  Speaker 1: example of interest. They have tested the placentas of males
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  Speaker 1: and females and found that the males tend to be
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  Speaker 1: a little bit more vulnerable to teratogenic effects, making them
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  Speaker 1: more susceptible to delaying of maturation of brain development over
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  Speaker 1: the course of time. Some of the teratogens include drugs, marijuana, cocaine.
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  Speaker 1: Also alcohol. You can think about fetal alcohol syndrome which
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  Speaker 1: impairs neural migration, having neurons moving from one place to another, microcephaly,
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  Speaker 1: the shrinking of the brain or the skull. Poor impulse control,
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  Speaker 1: which as we know as in the executive function area
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  Speaker 1: and the prefunnal cortex leads another one that disrupts synaptic
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  Speaker 1: growth and lowers IQ and increases risk of attention problems.
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  Speaker 1: Again in that prefunnel cortex area, maternal stress elevates cortisol,
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  Speaker 1: disrupts h PA access and affects fuel brain connectivity, so
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  Speaker 1: the HPA access to the stress system supporting to other
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  Speaker 1: timing and dosage of a triatogen exposure, which determines its
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  Speaker 1: effect early gestational exposures global brain late exposures localized impairments.
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  Speaker 1: If we go to early childhood brain development by h
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  Speaker 1: five of the brain is ninety percent of its adult size,
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  Speaker 1: but its connectivity, not size, determines function synaptic overproduction and pruning.
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  Speaker 1: Initially more connections of form than needed than through pruning,
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  Speaker 1: unused synapses are eliminated use it or lose it principle. Here,
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  Speaker 1: a lack of stimulation can result in excess pruning and
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  Speaker 1: reduce neural networks, something we saw with institutionalization. Myelination again
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  Speaker 1: is the fatty cloating or fatty fatty coating of axons
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  Speaker 1: that speeds up neural transmission. It's like a freeway. The
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  Speaker 1: myelination occurs in sensory motor regions first and continues into
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  Speaker 1: the pre cortex into the mid twenties, affecting impulse control
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  Speaker 1: and planning. See in adolescence, most of the brain structure already
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  Speaker 1: fully developed, which lacking is the connectivity. Highways aren't fully there.
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  Speaker 1: So all the streets are already developed, but that city
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  Speaker 1: doesn't have is the freeways fully developed Till your mid twenties.
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  Speaker 1: They estimate twenty four to twenty five. For the exam,
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  Speaker 1: you need to know the association in executive areas the
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  Speaker 1: mile and eight later. The deficits here are linked to ADHD,
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  Speaker 1: trauma and stress. So if you have terretogenic effects, this
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  Speaker 1: can delay the maturation of the prefunnel cortex area and
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  Speaker 1: the myelination sensitive periods and attachment. The brain's most responsive
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  Speaker 1: to positive or negative environmental input during early sensitive periods,
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  Speaker 1: so negative experience with abuse neglect equal Thinner cortexes reduce
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  Speaker 1: great matters for processings compromised a hyperactive amigala, so hypervigilance
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  Speaker 1: is going to be detective here. They're going to see
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  Speaker 1: threats where there are none positive so is the opposite.
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  Speaker 1: So when you have secure attachment strengthens the brain architecture
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  Speaker 1: and have a much healthier outlook for the exam no
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  Speaker 1: secure attachment and response caregiving and how they serve as
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  Speaker 1: protective factors against later psychopathology. Adolescence is marked by mismatch
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  Speaker 1: in brain maturation. The limbic system, rewarding emotions develop early
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  Speaker 1: prefunnel cortex judgment regulation matures into the mid twenties. This
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  Speaker 1: explains why risk taking happens pure influenced sensitivity, mood oder emergence,
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  Speaker 1: mood disorder, emergence, and impulsivity. Again, a lot of these
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  Speaker 1: areas are in the pre funnel cortex. As you mentioned,
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  Speaker 1: one thing you'll need to know nor that the reward system,
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  Speaker 1: the nucleo ciccumbents is highly active during adolescence. Teams are
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  Speaker 1: more reactive to novelty and immedia gratification. Again because the
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  Speaker 1: prefhoidal cortex highway isn't fully developed, so the emotions by
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  Speaker 1: the time they get to the pre formed to cortex
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  Speaker 1: to get a process, it's very slow biological and also
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  Speaker 1: you got to remember every adolescent it's different to the
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  Speaker 1: degree of this. That's why some adolescents may not be
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  Speaker 1: as impulsive as others or as risk takers as others.
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  Speaker 1: So it's going to be parenting the development better stronger
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  Speaker 1: development of their prefunnel cortex. There's a lot of factors here,
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  Speaker 1: the biological impacts of early stress and mountnutrition, HPA, access
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  Speaker 1: dysregulations of cortisol, overproduction, hippocampal damage, impaired feedback loops. Symptoms
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  Speaker 1: would include anxiety, effective instability, and memory problems AMIGDA overactivation
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  Speaker 1: heightens threat detection and emotional reactivity seen in PTSD, anxiety
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  Speaker 1: disorders and early trauma survivors, and once again, prefunnel cortex
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  Speaker 1: under development linked to poor at tension, impulse control and
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  Speaker 1: executive function, slower myelination and synapsformation due to poor nutrition
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  Speaker 1: or chronic stress. For you to pay attention to is
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  Speaker 1: know the timing is everything. Earlier exposures lead to more
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  Speaker 1: severe impairments neuer development to disorders, autism, spectrum disorder, core symptoms,
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  Speaker 1: social communication deficits, restrictive competitive behaviors. Neurological features include atypical connectivity,
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  Speaker 1: over connectivity in some areas, under connectivity in others, early
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  Speaker 1: brain overgrowth and frontal and temporal lobes, impaired mirror neuron systems,
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  Speaker 1: and genetic careriatabilities about eighty percent, So be ready to
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  Speaker 1: identify structural and functional brain differences in the amigala insulin
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  Speaker 1: mirror neuron deficits. No the role of early intervention remapping
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  Speaker 1: these circuits for the e triple p ADHD core problem.
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  Speaker 1: Delayed maturation of prefunnel cortex affecting attention and impulse control.
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  Speaker 1: You can see it overlaps quite a bit with autism,
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  Speaker 1: and we're seeing a lot of this comorbidity diagnosising. Now
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  Speaker 1: these codiagnosises, neurobiological findings activity and dorsal lateral prefunnel cortex,
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  Speaker 1: anterior singular, basal ganglia, cortical thickness, peak and activation and
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  Speaker 1: executive control networks. Pharmacological interventions stimulants which improve member dopamine
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  Speaker 1: and epidephrine transmission, also PFC activation combined with behavioral strategies
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  Speaker 1: that actually works much better being able to match the
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  Speaker 1: brain regions as functions, but symptoms are going to be
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  Speaker 1: good for the E triple P expect questions on how
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  Speaker 1: stimulants normalize under developed circuits in which neurotransmitters are involved.
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  Speaker 1: Don't forget the dopamine and nouro epinephrine for ADHD, as
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  Speaker 1: well as dorsal lateral prefunnel cortex, anterior cingulate, and the
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  Speaker 1: basal ganglia. So that starts covering a little bit of
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  Speaker 1: our biological for the development of the individual. Some other
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  Speaker 1: things I wanted to look at. We talked earlier about
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  Speaker 1: the reward center for the children or for adolescens. It's
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  Speaker 1: the nucleus incumbents is what you need to know is
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  Speaker 1: particularly active in adolescence. This makes teams highly responsive to
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  Speaker 1: novelty and immediate rewards, sometimes at the cost of long
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  Speaker 1: term consequence, and so prefundal cortex is also associated with
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  Speaker 1: anticipatory function, so anticipating what could happen, and the MRI's
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  Speaker 1: adolescents reward circuits light up faster and more intensely than
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  Speaker 1: control networks, which is no surprise. The prefundal cortec doesn't
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  Speaker 1: fully catch up until the mid twenties, which is that
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  Speaker 1: which has implications for treatments, legal policy, and education. So
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  Speaker 1: it's important to know that when we look around, let's
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  Speaker 1: see if there's anything else I've missed well, from fetal
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  Speaker 1: brainstem formation to adolescent prefrontal pernium, the trajectory of brain
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  Speaker 1: development is anything but linear. Just remember its shaped like timing,
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  Speaker 1: experience and interaction between biology and environment. So make sure
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  Speaker 1: you understand that. And that's it for today. We're going
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  Speaker 1: to be talking about tomorrow or next week. Actually we'll
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  Speaker 1: take this week this weekend off. Psychoeurominology and the biology
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  Speaker 1: of stress is our next ones. We'll be looking at
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  Speaker 1: the immune system and how it associates with psychology and
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  Speaker 1: the nervous system. It won't be recording on the weekends.
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  Speaker 1: So what you can do is go back and revisit
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  Speaker 1: this week's lectures, and as the weeks go on, you
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  Speaker 1: can revisit from the beginning, so you have plenty of material.
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  Speaker 1: Hopefully the months go forward. We should be doing this
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  Speaker 1: probably for three or four months, and then if people want,
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  Speaker 1: we'll go into advanced stuff into these areas and maybe
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  Speaker 1: that'll help you better understand some of the concepts. If
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  Speaker 1: you're don't