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Neurodevelopmental Determents MH > Exam Slides > Flashcards

Exam Slides Flashcards

1
Q

4 symptoms of SCH

A
  • Delusions
  • Hallucinations
  • Disorganized speech
  • Alterations in executive functions
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2
Q

The age of onset of SCH coincides with what?

A

The maturation of the PFC

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3
Q

What is the cause of SCH

A

Unknown

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4
Q

What are the 4 main hypotheses of SCH

A
  1. Neurodevelopmental
  2. Dopamine
  3. Hypofrontality
  4. Glutamate
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5
Q

What is the environmental model of SCH

A

Suggests that the late onset is caused by the increased cognitive and social demands of that stage of life

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6
Q

What are the genetic models of SCH

A

Suggests that there could be a genetic basis, and that genes may interact with the environment

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7
Q

What is the neurodevelopmental model of SCH

A

Suggests that disrupted/abnormal brain development could cause SCH and it only becomes apparent later when those brain areas are needed/matured

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8
Q

Heterogeneity genetic contribution to SCH

A

It is separate distinct diseases, each inherited based on specific gene mutations

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9
Q

Monogenetic genetic contribution to SCH

A

A dominant single gene mutation resulting in highly variable phenotypic expression

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10
Q

Polygenetic genetic contribution to SCH

A

The phenotype is caused by multiple gene mutations

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11
Q

Combinatorial model of genetic contribution to SCH

A

It results from complex interactions between genetic susceptibility and environment

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12
Q

What receptor is thought to be involved in SCH

A

D2 receptor

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13
Q

What is the issue with the D2 receptor in SCH

A

it is overactive

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14
Q

What is the evidence that supports the dopamine hypothesis of SCH

A

D2 receptor agonists are effective in the treatment of some people with SCH

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15
Q

What is the neurodevelopmental hypothesis of SCH

A

Brain abnormality present at or shortly after birth is “unmasked” as a result of normal maturation events that occur in late adolescence and early adulthood

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16
Q

What are the 7 stages of neurodevelopment

A
  1. Neurogenesis
  2. Migration
  3. Growth of axons
  4. Synaptogenesis
  5. Synaptic pruning
  6. Neuronal death
  7. Myelination
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17
Q

Emergence of SCH symptoms correlate with the stage of development occupied by significant __________

A

synaptic pruning

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18
Q

Abnormalities to what gene has been associate with the symptomology of SCH

A

DISC-1

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19
Q

The DISC-1 gene is involved in what brain process?

A

Glutamate

–> Neurotransmission and plasticity

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20
Q

What brain region is DISC very active in?

A

Forebrain

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21
Q

DISC-1 is highly expressed in areas where there is what?

A

Neurogenesis

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22
Q

DISC-1 interacts with many proteins and plays a role in (3)

A
  • Neuroplasticity
  • Axon growth
  • Neural migration
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23
Q

In SCH there is an issue with ________ and a lower number of ________

A

Synaptic elimination

Dendritic spines

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24
Q

SCH is considered a disorder of _______

A

cortical connectivity

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25
Q

What are the 2 types of imaging to detect SCH

A

Diffusion tensor imaging and fMRI

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26
Q

What brain region seems most affected in SCH

A

Frontal lobe

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27
Q

Stage 1: Presymptomatic SCH

A

<15 y

The negative symptoms start

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28
Q

Stage 2: Prodrome SCH

A

15-18y

Cognitive and social deficits

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29
Q

Stage 3: Psychosis SCH

A

18-25 y

Diagnosis and start to see positive symptoms

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30
Q

Stage 4: Chronic illness SCH

A

> 25y

Positive and negative symptoms, start to seek treatment

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31
Q

What are the 3 types of treatment for chronic SCH

A

Medical
Psychological therapy
Rehabilitation

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32
Q

During stage 3 of SCH, what starts to be seen in the brain in terms of grey matter

A

Deficient myelination and excessive excitatory pruning

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33
Q

There is decreased white matter in what brain regions in SCH

A

Frontal lobe
Cerebellum
Limbic structures

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34
Q

What NT are altered in SCH

A

Dopamine
Serotonin
Glutamate

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35
Q

There are brain abnormalities in what 2 brain regions in SCH

A

PFC

Hippocampus

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36
Q

3 brain pathology in SCH

A
  1. Lateral ventricle enlarged
  2. Reduced brain volume (particularly grey matter)
  3. Abnormal/reduced neuronal complexity
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37
Q

Abnormal neurodevelopment results in _______ dopamine activity in the _______ in SCH

A

excessive

limbic system

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38
Q

Abnormal neurodevelopment results in ________ activation within the ______ in SCH

A

Reduced

Prefrontal cortex

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39
Q

What are the 3 things that result from hypofrontality in SCH

A
  1. Lower frontal lobe activity
  2. Reduces axon density in the PFC
  3. Reduced dopamine in the PFC
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40
Q

Abnormal limbic system = _______ symptoms SCH

A

positive

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41
Q

Abnormal PFC = _______ symptoms in SCH

A

negative

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42
Q

What type of life events have been correlated with the onset of SCH

A

stressful

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43
Q

What happens to a person with SCH when they get stressed

A

Their symptoms get worse

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44
Q

Stress response mechanisms appear to be ______ in some people with SCH

A

abnormal

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45
Q

What are the 2 types of medication for treating SCH

A

Typical and atypical antipsychotics

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46
Q

What is the main atypical antipsychotic

A

Clozapine

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47
Q

What is Clozapine reserved for?

A

Patients with treatment resilience

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48
Q

Why isn’t Clozepine used more often in people with SCH

A

It has sever side effects like agranulocytosis and seizures

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49
Q

Agranulocytosis

A

lower production of white blood cells

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50
Q

Without medication, schizophrenics relapse at a rate of _____ within the first year of diagnosis

A

60-70%

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51
Q

Damage to what area of the brain has been shown to have masked effects of depression until 2 y in monkeys

A

Dorsolateral prefrontal cortex

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52
Q

What is the cause of mood disorders?

A

Unknown

Thought to maybe be affected by biological, psychological and social factors

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53
Q

What are the 2 main types of depression

A 
Major depressive disorder
Bipolar disorder (depression and mania)
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54
Q

What is the prevalence of depression in women compared to men?

A

Women are 2x as likely

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55
Q

What is the most common type of mood disorder

A

depression

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56
Q

What are the 2 major types of mood disorders

A

Depression

Mania

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57
Q

Diagnosis of depression depends on what two things?

A

Symptoms and the duration of the symptoms

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58
Q

What is diagnosis of depression often based on?

A

Self report

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59
Q

What demographic is most likely to get depression

A

Women of child-bearing years

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60
Q

Major depression:

A

Exhibit episodes of depressed mood for 2+ years

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61
Q

what is a major physiological disturbance of major depression

A

sleep problems

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62
Q

What characterizes bipolar disorder

A

the presence of one or more manic episodes

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63
Q

The exact consequence of maternal depression on the child depends on what

A

the specific stage of development that the disruptions occured in

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64
Q

Children of depressed mothers often show these 6 characteristics

A
  1. More drowsy or fussy
  2. Less relaxed or content
  3. Engage in less toy exploration
  4. Less focused play
  5. Rated as crying more, difficult to sooth
  6. Higher rates of psychiatric illness at school age
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65
Q

What 3 factors might cause the effects of maternal depression on the child

A
  1. Genetics
  2. Prenatal environment
  3. Parenting style/home environment
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66
Q

Prenatal stage effects of maternal depression (4)

A
  • Poor nutrition
  • Inadequate prenatal care (not taking vitamins)
  • higher preterm birth and low birth weight
  • higher incidence of spontaneous abortion
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67
Q

Maternal depression effects/symptoms of infants (3)

A
  • Anger and protective style of coping
  • Passivity and problems with attention
  • Lower cognitive performance compared to peers
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68
Q

The effects on toddlers with depressed mothers (2)

A
  • Less mature expression of autonomy and lower peer interactions
  • Cognitive: less creative play and lower cognitive performance
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69
Q

Developmental effects of adolescents with depressed mothers (4)

A
  • Difficulty adapting to new situations
  • Affective disorders, anxiety, conduct disorders and panic disorders
  • ADHD and learning disorders ***
  • Higher incidence of substance abuse and alcohol dependence
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70
Q

What is the genetics of depression

A

There has been no clear link found

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71
Q

What is the current focus in research on genes in childhood depression

A

Trying to see what depression looks like in children and find potential risk factors

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72
Q

Epigenetic effects of a depressed mother

A

Could inherit an abnormal stress response

Mother’s depressive behaviours can train the child’s brain to act in a certain way to a stressor

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73
Q

What is the controversy in diagnosing depression in children

A

Do not want to label them that young

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74
Q

What medical treatment for depression works in adults but not in children or adolescence

A

Tricyclic anti-depressants (TCA)

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75
Q

What drug treatment is more effective with some children and adolescents with depression

A

SSRIs

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76
Q

What is the main SSRI drug

A

Fluoxetine

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77
Q

Other than affect serotinin, what do SSRIs do?

A

They can induce epigenetic factors (increase neuroplasticity)

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78
Q

Differences in action of SSRI verses TCA could provide clues on _________ pathogenesis of depression

A

early-onset

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79
Q

How do TCAs and SSRIs increase NT

A

block reuptake

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80
Q

How do MAOIs increase NT

A

inhibit breakdown

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81
Q

What techniques is used to study sleep?

A

EEG –> monitors brain waves

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82
Q

What are the 5 sleep alterations in depressed children and adolescents

A
  • Sleep continuity disturbance
  • Reduced time until REM stage
  • Increased time spent in REM stage
  • Decreased delta waves (stage 3 and 4 sleep)
  • Difficulty waking up
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83
Q

Paroxetine (Paxil) is what type of drug

A

Anti-depressant

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84
Q

Why are TACs not used in children and adolescents

A

They are not very effective

They can cause severe side effects (even death)

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85
Q

There are higher levels of what in adults with depression

A

Cortisol during the day and night

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86
Q

About __% of depressed adults show hyper cortisol secretion

A

50`

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87
Q

Do depressed children show excess cortisol

A

Not usually

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88
Q

In depressed adults and children there is decreased volume of _____ and decreased volume of _____ only in adults

A

Amygdala

Hippocampus

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89
Q

What are the 4 neurological characteristics associated with depressed adults

A
  1. Excess cortisol
  2. Reduced size of frontal lobe and amygdala
  3. Hippocampal atrophy
  4. Abnormality in orbitofronal cortex linked to early onset
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90
Q

Abnormality in what brain region has been linked with early onset of depression? What does this result in?

A

Orbitofrontal cortex

> Abnormal serotonergic function

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91
Q

What is used to test white matter abnormality?

A

Diffusion tensor imaging

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92
Q

What is DTI used for

A

It evaluates the integrit of white matter tracts

>Specifically subcortico structures

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93
Q

DTI has shown what is depressed in individuals

A

Abnormality in the corpus callosum

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94
Q

What gene is implicated in SCH that might also be implicated in bipolar disorder

A

EGR3

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95
Q

What CNS protein does EGR3 affect?

A

BDNF

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96
Q

Lower EGR3 leads to _____ BDNF

A

reduced

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97
Q

What is the direction of the relationship between EGR3 and BDNF

A

Bi-directional

They affect each other

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98
Q

What are the brain effects of reduced EGR3? (2)

A
  1. Impaired neuroplasticity and resilience

2. Increased vulnerability to stress

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99
Q

Prevalence of down syndrome

A

1 in 1000

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100
Q

What are the 2 gender differences in DS

A
  1. More in males

2. Higher infant mortality in females

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101
Q

What is the first prenatal test for DS? Then what happens?

A 
Nuchal translucency (ultra sound)
>> If it indicates DS then other tests like karyotyping are performed
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102
Q

What does karyotyping test/

A

The number and structure of chromosomes

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103
Q

Probability of infant having DS increases with mother’s ___

A

age

|&raquo_space;But this is going down

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104
Q

Aneuploidy =

A

abnormal number of chromosomes

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105
Q

What is the problem with aneuploidy in DS?

A

There is an “over-expression” of many genes and proteins

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106
Q

What are the 2 types of aneuploidy in DS, what are the prevalences

A 
Complete trisomy (95%)
Mosaic or partical trisomies (5%)
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107
Q

What are the 2 hypotheses for DS

A
  1. Gene dosage effect hypothesis

2. Amplified developmental instability hypothesis

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108
Q

What is the gene dosage effect hypothesis

A

The extra distal genes on the 21st chromosome (DSCR genes) that are present in DS are important for regulating neurodevelopment. The presence of the extra genes can disrupt development and cause specific DS phenotypic traits

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109
Q

The severity of DS according to the gene dosage effect depends on what?

A

The extent of trisomy in the DSCR

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110
Q

What is the amplified developmental instability hypothesis

A
  • DS phenotypes result from the elevated activity of specific genes (DSCR) that result in the over production of DSCR proteins, which in turn cause global disruption of protein homeostasis

> Causes pervasive developmental instability/ abnormality

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111
Q

Full trisomy =

A

Complete extra chromosome

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112
Q

Partial trisomy =

A

One part of chromosome 21 moves to another chromosome

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113
Q

Mosaicism -

A

Still see trisomy 21, but only in some cells

|&raquo_space; Error in cell division after fertilization

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114
Q

What are the cognitive abilities with ppl with Mosaicism DS

A

They have higher mean cognitive scores than those with full trisomy

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115
Q

How could XIST, the X-inactivation gene, be potentially used to treat DS?

A

XIST activation produces RNA that coats the surface of the chromosome 21.

–> Blocks genes on the extra chromosome 21 from being accesses and thus suppresses expression

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116
Q

When would XIST have to be given to be an effective treatment for DS?

A

Early in development to try to normalize the expression of genes

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117
Q

Brushfield spots =

A

White spots in the iris of the eye

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118
Q

What disorder are brushfield spots associated with?

A

Down Syndrome

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119
Q

What disorder is commonly present in DS that is also present in a lot of neurodevelopmental disorders?

A

Gastrointestinal issues

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120
Q

What are the 2 ways that trisomy 21 interferes with the fetal nervous system development

A
  1. Reduction in total numbers of neurons in cortical areas

2. Proposed “accelerated aging”

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121
Q

What is the trend of brain weight for ppl with DS

A

Tends to fall below average

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122
Q

What are the 2 structure/function of neurons in DS

A
  1. Reduced neuronal density (especially in cortical areas)

2. Poop synaptic connections

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123
Q

4 difficulties in learning and cognitive processing of DS

A
  • Attention
  • Info processing
  • Short and long term memory processing
  • Language skills
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124
Q

What do MRI scans of ppl with DS show? 3

A

Generalized atrophy:

  • Smaller total brain size in adults
  • Smaller size of the hippocampus and amygdala
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125
Q

6 Co-Morbidities of DS

A
  • Alzheimers
  • ADHD
  • Aggressive behaviours
  • Anxiety disorders
  • Self injury
  • Autism spectrum disorder
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126
Q

Growth and stature appear “normal” during the first ________ of life in ppl with DS

A

3 years

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127
Q

When is DS typically diagnosed?

A

35% at birth
46% by 2 years
Very small number after 3 years

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128
Q

In addition to Karyotyping, what other things are screened for when there is the potential for DS (4)

A
  • Cataracts
  • Blockages in gastrointestinal tracts
  • Congenital heart disease
  • Hearing problems
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129
Q

Are there pharmacotherapies for DS

A

Nothing to directly treat DS, but there are medications to treat the co-morbid symptoms (ADHD, aggression)

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130
Q

What is the treatment focus for DS?

A

Social, emotional, cognitive and motor abnormalities

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131
Q

What are 4 medical / social concerns for people with DS

A
  • Independent living and employment challenges
  • Difficulty developing social skills
  • Improvement in symptom management has resulted in longer life (more time being dependent)
  • Neurodegeneration (AD) is common
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132
Q

What is implicated in both DS and Alzheimers disease?

A

Amyloid precursor protein (APP)

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133
Q

Why is there such a high prevalence of Alzheimers in ppl with DS

A

Because the APP gene is located on Chromosome 21, and it is triplicated in DS

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134
Q

What does a brain of a person with DS look like in comparison with Alzheimers?

A

Even more cortical atrophy

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135
Q

What are the two directions of axonal transport

A

Anterograde and retrograde

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136
Q

Anterograde transport:

A

Transportation from the cell body to the terminal

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137
Q

Retrograde transport:

A

Transportation from the terminals to the soma

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138
Q

Which type of axonal transport is affected in DS

A

Retrograde

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139
Q

Why is retrograde transport affected in DS?

A

Because the excess of APP causes enlarged endosomes, and they block the axon so things cannot pass them

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140
Q

What is the animal model for DS, specifically for retrograde transport problems?

A

Ts65Dn mice

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141
Q

Why is abnormalities in retrograde transport a problem?

A

Because then the axon cannot communicate with the soma, it cannot tell it what it needs so there might be the over or under production of proteins

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142
Q

PKU is the mutation in the gene from what enzyme?

A

Phenylalanine Hydroxylase (PAH)

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143
Q

What does PKU stand for

A

Phenylketonuria

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144
Q

What genetic inheritance pattern does PKU follow?

A

Autisomal recessive

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145
Q

Other than genetics, what can PKU be caused by?

A

Abnormals levels of dietary phenylalanine

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146
Q

What is phenylalanine? What is it classified as?

A

An essential amino acid

Classified as a Large, Neutral Amino Acid (LNAA)

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147
Q

What are essential amino acids?

A

Amino acids that you can only get from your diet

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148
Q

The mutation if PAH impaired the conversion of phenylalanine to _________

A

Tyrosine

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149
Q

What is tyrosine essential for creating in the body?

A

Dopamine

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150
Q

If you don’t have PAH enzyme or it is dysfunctional, it can results in excess ______ . Why is this bad?

A

Phenylpyruvic acid

> > Can be toxic

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151
Q

What 2 metabolic things cause most if the symptomology of PKU

A

Excess phenylpyruvic acid

Lack of dopamine

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152
Q

DOPA (dopamine) is also involved in the production of what? What does this phenotypically result in in the brain?

A

Melanin pigments

Results in the lighter coloured dopamine cells

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153
Q

How is PKU detected? When is this done?

A

A blood test

Done right after birth (heel prick)

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154
Q

Why is early detection of PKU important

A

Early treatment prevents associated intellectual disabilities

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155
Q

If PKU is not treated, what metabolites can be seen in the blood and urine?

A

Urine : phenylpyruvic acid

Blood : Phenylalanine

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156
Q

If PKA is left untreated, what problems occur

A

Intellectual disability/mental retardation

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157
Q

Research suggests that increased levels of what in blood contribute to the neuropsychological deficits in PKU

A

Phenylalanine metabolites

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158
Q

What are the names of the 3 neuropsychological hypotheses in PKU

A
  1. Myelin synthesis and turnover
  2. Competition for transport
  3. Dopamine reduction
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159
Q

Myelin Synthesis and Turnover PKU Hypothesis

A

High levels of phenylalanine or metabolites inhibit myelin development

> > There is a delay in development of myelin and there is myelin degradation in ppl with PKU

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160
Q

What do imaging techniques show in the brains of people with PKU

A

Reduction in white matter (myelin)

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161
Q

What causes the degradation of myelin in PKU

A

Phenylpyruvic acid

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162
Q

Is it maternal or infant diet that has the most effect on PKU? Why?

A

Infant, because most myelination happens post natally

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163
Q

What is the Competition for Transport Hypothesis Hypothesis (3)

A

Phe competes with other essential amino acids for transport across the BBB

Phe tends to have a higher affinity for transporter than other LNAA

Results in an accumulation of Phe in the bloodstream and other amino acids cannot come into the brain because the Phe is tying up all the transporters

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164
Q

What other essential acid cannot enter the brain in PKU? What NT requires it?

A

Tryptophan

Serotonin

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165
Q

What is the dopamine Reduction Hypothesis of PKU

A

Phenylalanine is not converted to tyrosine in the absence of PAH, which results in a lack of dopamine

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166
Q

What is the effect of the lask of dopamine in PKU

A

It effects the prefrontal cortex, which impacts executive functions

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167
Q

Why is it difficult to make an animal model of PKU

A

Because there are over 600 possible mutations on the PAH gene

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168
Q

What is the phenotypes of the PKU animal model with a mutation in the PAH gene? (2)

A
  1. Lighter coloured coat (because of the tyrosine –> melanin pigment deficiency)
  2. Abnormal motor skills (inability to swim)
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169
Q

What treatment of the PKU mice result in noticable changes

A

Phe-restricted diet

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170
Q

How is myelin affected in PKU (2)

A
  1. Delayed development

2. Demyelination

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171
Q

What dietary compound contains a LOT of phenylalanine

A

Aspartame (“diet” food)

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172
Q

Early treatment with Phe-restricted diet reduces the ________ manifestations of PKU

A

Behavioural

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173
Q

2 individual differences in ppl with PKU

A
  1. Some do not respond to treatment

2. Some with high levels of phenylalanine metabolites do not suffer neurological impairment

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174
Q

Which chromosome is the PAH gene on

A

12

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175
Q

Classical PKU

A

No PAH activity, enzyme is formed but not effective

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176
Q

Mild PKU

A

~25% residual PAH activity

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177
Q

Severity of PKU depends on ________

A

Genotype

> whether there is some residual PAH activity

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178
Q

What is the main treatment for PKU

A

Phe restricted diet

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179
Q

What foods are permmited in a Phe restricted diet? (2)

A
  1. Measures amounts of fruits and vegetables

2. Low protein: pasta, grains, and breads

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180
Q

What foods are not allowed in Phe restricted diet (6)

A 
Meat 
Fish 
Eggs 
Dairy 
Nuts 
Soy
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181
Q

What happens when a person with PKU strays from the diet

A

They become fatigued and start showing signs of cognitive deficits

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182
Q

How does BH4 PKU therapy work?

A

BH4 boosts the activity of PAH, in individuals with residual PAH activity

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183
Q

How does LNAA supplemental therapy work for PKU

A

The LNAA comete with Phe to cross the BBB which allows for more amino acids to enter the brain

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184
Q

What is Glycomacropeptide

A

A Phe-free source of protein

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185
Q

PFC in PKU

A

Pattern of deficits affecting projections of dopamine neuron in the frontal lobe, resulting in cognitive problems

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186
Q

What is the probable cause of the cognitive deficits in PKU

A

Myelin abnormalities

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187
Q

What imaging technique best shows white matter in the brain

A

DTI

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188
Q

What are the 2 essential and one non-essential amino acids we need to know

A

Essential:
- Phenylalinene and Tryptophan
Non-Essential:
- Tyrosine

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189
Q

Fear

A

Negative neurological state brought on by perceived presence of threatening stimuli

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190
Q

Anxiety

A

Neurological state “engages” when encountering sustained cues that may predict a threat

191
Q

GAD

A

Generalized anxiety disorder

192
Q

Specific Phobia

A

Clinical presentation of anxiety as a result of exposure to a “feared” object or situation

193
Q

What demographic typically has a panic disorder

A

Younger people

194
Q

Panic Disorder

A

Sudden onset of intense fear and apprehension, impending doom

195
Q

4 categories of anxiety disorders

A

Social phobia
PTSD
Acute stress associated with anxiety
Separation anxiety

196
Q

Anxiety disorder is where a person experiences ____ anxiety when separated from _____ and ______

A
  1. Excessive
  2. Home
  3. Parent
197
Q

What is separation anxiety predictive of?

A

Other anxiety-related issues

198
Q

Behavioural inhibition:

A

Long latency to speak, play or interact with strangers

199
Q

Behavioural inhibition is predictive of what?

A

Future anxiety disorders

200
Q

Pleasant emotions activate what hemisphere?

201
Q

Negative affect activates what hemisphere

202
Q

People with anxiety have higher levels of activation of which hemisphere?

203
Q

Family pattern of anxiety

A

Higher rates of anxiety in children whose parents have anxiety

204
Q

Mice lacking ______________ show increased anxiety

A

5HT-1A auto-receptors

205
Q

5HT-1A regulate the release of what?

206
Q

In rat pups raised by inattentive moms, what three things are seen in the pup?

A
  1. Highly reactive HPA axis
  2. Increased plasma cortisol levels
  3. Reduced 5-HT levels
207
Q

What is the relationship between levels of cortisol and the levels of serotonin?

A

Increased cortisol can decrease the amount of serotonin

208
Q

This balance of cortisol and serotonin is seen especially where?

A

In brain areas involved in the HPA axis

209
Q

What is the medical name and the shelf name of the most common SSRI

A

Fluoxetine

Prozac

210
Q

What psychological therapy is best for anxiety disorders?

211
Q

When pharmocotherapy and CBT are used together, what NT is affectes

A

SSRIs can enhance tropic factors in the brain (BDNF)

212
Q

Why does it take a while to see the effects of SSRIs

A

Because it takes time for the trophic factors to become activated

213
Q

ASD is characterized by varying degrees of impairment in: 3

A

Social interaction
Communication skills
Pre-occupation with a single subject or activity

214
Q

The term “autism” was first used to depict the tendency of ______ to isolate themselves and focus on their inner life

A

schizophrenics

215
Q

3 characteristics of social impairment in ASD

A
  1. Do not like to be picked up/cuddled
  2. Rarely smile/laugh in response to stimuli
  3. Prefer “interacting” with objects
216
Q

2 characteristics of communication impairment of ASD

A
  1. High incidence of being mute

2. Robotic behaviour- interacting more with objects

217
Q

2 repetitive and stereotypes behaviour patterns of ASD

A
  1. Flapping hands, rocking/twirling repeatedly

2. Restricted interest - less “creative play” with objects

218
Q

Autistic savant

A

Person with autism having abnormally high skill in one area

219
Q

2 abnormal sensory perceptions in people with ASD

A
  1. Either hyper or hypo-responsive to stimuli

2. Synaesthesia

220
Q

Typical Autism

A

Impairment across all core symptoms

221
Q

4 core symptoms of typical autism

A
  1. deficits in social functioning
  2. Lack of emotional reciprocity
  3. Impaired verbal and non-verbal communication
  4. Repertoire of repetitive, restrictive and stereotyped behaviours
222
Q

Atypical Autism

A

Impairment in all three core domains, but full diagnostic criteria for pervasive developmental disorder (PPD) not met

223
Q

3 core domains in atypical autism

A
  1. No significant cognitive impairment
  2. No significant abnormality in language development
  3. “intact” social skills
224
Q

Is atypical autism more mild then typical autism?

A

Not necessarily

225
Q

“Low functioning” autism refers to being _____ responsive

226
Q

“High functioning” autism refers to being _____ responsive

227
Q

High functioning autistics usually have _____ average intelligence and low function usually have _____ average intelligence

A

Above

Below

228
Q

Often children with autism start developing normally and then what?

A

There is noticeable impairment between 2 and 3

229
Q

What 3 impairments appear at 2-3 in autism

A
  1. Deterioration in language skills
  2. Loss or impairment in social behaviour
  3. Onset of stereotypes or repetitive behaviours
230
Q

Most of the cases of autism are ___ cause

A

idiopathic

231
Q

Environmental toxin OR genetic abnormality are associated with ____% of autism cases

232
Q

There is a high incidence of what brain abnormality with autism

A

Microcephaly

233
Q

Complex autism:

A

evidence of some abnormality of early brain development

234
Q

Essential autism:

A

met the diagnostic DSM5 criteria for autism

> No obvious brain abnormalities

235
Q

There is a suggested chromosomal abnormality is ___% cases of autism

236
Q

What genes are involved in autism

A

Unknown but it is thought to be polygenic

237
Q

5 Environmental factors associated with autism

A
  1. Prenatal infections (viral)
  2. Peri-natal brain damage
  3. Heavy metal exposure
  4. Pesticide/herbicide
  5. BPA
238
Q

What heavy metal might be associated with autism

239
Q

What is the controversial chemical in vaccines that “might” be associated with autism

A

Thimerosal

240
Q

What is the active ingredient in weed killer that has been “associated” with autism

A

glyphosate

241
Q

High levels of what NT at birth has been associated with autism?

242
Q

Why is it thought that high levels of BDNF in the blood at birth could be associated with autism

A

BDNF that is produced in the brain might be leaking out so there is not enough in the brain to facilitate proper growth and protection

243
Q

2 teratogins that have been linked to autism

A
  1. Alcohol

2. Valproic acid (mood stabilizer)

244
Q

Greater frequency in ________ disease in families with high prevalence of autism

A

autoimmune

245
Q

What antigen might be implicated in autism?

A

Human leukocyte (HLA)

246
Q

Abnormalities in the function of 3 cytokines/chemokines have been suggested to be linked with autism

A
  1. Interleukins
  2. TNF
  3. Interferon gamma
247
Q

Cerebral volume in autism (3)

A
  1. Smaller cell size
  2. Increased cell density
  3. Premature over production of neurons
248
Q

Amygdala in autism

A

Difficulty with emotional response

249
Q

Hippocampus in autism (3)

A
  • enlarged
  • smaller neurons
  • cells packed more densely
250
Q

Serotioin in autism

A

Levels are elevated

251
Q

Why are there higher incidence of seizures and anxiety disorders in people with autism

A

Because there is an imbalance in GABA and Glutamate

252
Q

What are mirror neurons essential for? (3)

A

1 Ability to understand and imitate others’ actions
2 Allows for empathy
3. Facial and emotion recognition

253
Q

Where are mirror neurons typically locate? (2)

A

Inferior motor cortex

Superior parietal lobe

254
Q

There are no drugs that directly treat autism, but there are drugs that treat the associated symptoms, what are they (4)

A

Haloperidol
Risperidone
Methylphenidate
SSRIs

255
Q

What type of drug is haloperidol and what is it used for in autism

A

Typical antipsychotic

Used to treat aggression and hyperactivity

256
Q

What type of drug is risperidone and what it is used to treat in autism?

A

Reduction in irritability, aggression and injury

257
Q

Risperidone affects what NT

258
Q

What is methylphenidate used for in autism

A

Treat ADHD symptoms

259
Q

What are SSRIs used for in autism (2)

A
  • Decrease repetitive behaviours

- Improve language and social skills

260
Q

What alternative medicine is used to treat autism

A

Managing diet to target gastrointestinal problems

261
Q

What is the most common MONOgenic inheritable form of mental retardation

A

Fragile X Syndrome

262
Q

FXS is inherited from an error in what gene

263
Q

What protein is affected in FXS

264
Q

Is FXS more common in males or females

265
Q

Broad spectrum of disabilities for FXS (3)

A
  • Learning disabilities
  • Mild to moderate intellectual disabilities
  • Cognitive impairment
266
Q

~____% of people with FXS show autistic characteristics?

267
Q

4 physical features of FXS

A
  • Pong/prominent ears
  • Long face
  • Flat feet
  • Cardiac murmur
268
Q

What is Fragile X-associated primary ovarian insufficiency

A

Ovarian cysts and premature menopause in women

269
Q

3 Behavioural features of FXS

A
  • Short attention span
  • Impulsivity
  • Hyperactivity
270
Q

What is the abnormal amino acid repeats on the FMR1 gene

271
Q

Normal CGG repeats on FMR1

272
Q

Pre-mutation CGG repeats on FMR1

273
Q

Full mutation CGG repeats on FMR1

A

more than 200 repeats

274
Q

What is the normal function of CGG repeats on the FMR1 gene

A

Recruiting methylation (silencing) groups

275
Q

The more CGG results in more _____ with causes ______ FMRP to be made

A

Methylation/Silencing

less

276
Q

How much FMRP is made in pre-mutation FXS

A

Less than normal protein made

277
Q

How much FMRP is made is full mutation FXS

A

No protein made

278
Q

FXS is more sever in males or females? Why?

A

Males
It is an X linked disorder, and males have only one X chromosome, so there is nothing to compensate for the mutated chromosome

279
Q

3 possible inheritance patterns with FXS carrier parent

A

Normal
Pre-mutation
Full mutation

280
Q

CGG repeats are located where on the FMR1 gene?

A

Front end, in the promoter regions

281
Q

What does it mean for transcription that the CGG repeats are at the promotor region of the gene in FXS?

A

Transcription factors are inhibited from binding to the DNA so transcription cannot happen

282
Q

What is FXTAS?

A

Fragile X associated tremor/ataxia syndrome

|&raquo_space;Late onset neurodegenerative disorder

283
Q

What form of FXS can FXTAS occur in?

A

Pre-mutation and full mutation

284
Q

What cellular function is FMRP integral for?

A

RNA transport and regulation

285
Q

What are the intranuclear inclusions in FXTAS made of?

A

Pre mutation –> RNA and abnormal FMRP build up

Full mutation –> just RNA build up

286
Q

Why do the intranuclear inclusions happen in FXTAS?

A

FMRP is supposed to regulate the production of RNA and RNA transport, but when there is not enough if it, RNA gets over produced and it is not able to exit the nucleus, so it builds up

287
Q

What is the late onset neurodegenerative disease that is associated with FXS

288
Q

Many ____ mutation patients develop FXTAS

A

pre-mutation

289
Q

FMR1 pre-mutation carriers show intra-nuclear brain inclusions that can result in (3)

A
  1. Parkinsons
  2. Motor abnormalities
  3. Significant cognitive deficits
290
Q

FMRP deficiency results in dysregulation in:

A

global protein expression in the brain

291
Q

What are mGluR5? What do they do (2)

A

Metabotropic Glutamate Receptor

  1. Function in synaptic plasticity and learning
  2. Longer term depression
292
Q

What disorder is long term depression commonly seen in

293
Q

FXS often causes more or less mGluR5 in the brain? What does this result in?

A

More

Results in too many synaptic sites

294
Q

There is an __________ of synpatic spines in FXS but they are ________

A

Over-abundance

Immature

295
Q

Long term potentiation (LTP)

A

Long term strengthening of synaptic interaction between neurons

296
Q

Long term depression (LTD)

A

Weakened synaptic strength between neurons

297
Q

In FXS, long term depression promotes what?

A

Weak synaptic connections

298
Q

Relationship between mGluR5 and long term depression

A

More mGluR5 results in enhanced LTD because even though there are lots of connections, they are weaker connections

299
Q

Why is it that as people with FXS age they have degreased cognitive abilities?

A

More neurodegeneration from the intranuclear inclusions

300
Q

What 2 brain areas are enlargened in people with FXS

A

Caudate and thalamus

301
Q

What could the enlarged caudate explain?

A

the ADHD symptoms

302
Q

People with FXS are often misdiagnosed as having

303
Q

What is the treatment for FXS

A

No cure so the treatment is for symptoms

304
Q

What atypical antipsychotic drug can be used for FXS

305
Q

The drug minocycline is though to reduce what in FXS

A

Reduce matrix metalloporteinase 9 (MMP-9)

306
Q

MMP levels are high in the absence of ____

307
Q

High levels of MMP-9 is correlated with what?

A

Brain damage q

308
Q

FMRP regulates the ____ protein

309
Q

What is the function of APP?

A

It regulates the number of spines on dendrites

310
Q

More APP in people with FXS is related to what? (3)

A
  • Alzheimer’s disease
  • Increased intellectual disability
  • More immature spines
311
Q

Lack of FMRP leads to ______ BRD4

312
Q

What layer of primordial tissue develops into the nervous system?

313
Q

What 3 things does the ectoderm develop into

A
  • CNS
  • PNS
  • Skin
314
Q

what is the process of gastrulation?

A

Blastula will invaginate and then close up to form the neural tube

315
Q

What is the notochord?

A

Area under the neural tube that is important in sending the signals for the development of the nervous system

316
Q

3 stages of neural tube

A

Neural plate –> neural crest –> neural tube

317
Q

What week does gastrulation occur?

A

~3rd week of pregnancy

318
Q

When does neurolation occur?

A

within the first 4 weeks of pregnancy

319
Q

What is the implication of gastrolation and neurolation happening so soon in the pregnancy

A

The women might not know she is pregnant yet so she is not living the best lifestyle

320
Q

Anencephaly

A

Absence of major portion of the brain/skill

321
Q

What is the prognosis of anencephaly?

A

Early mortality

Baby does not make it to term or dies soon after birth

322
Q

Spina bifida

A

Incomplete closure of the neural tube

323
Q

What is the most common form of spina bifida

A

myelomeningocele

324
Q

What are the 2 broad categories of spina bifida?

A

Occulta

Cystica

325
Q

What is spina bifida occulta

A

Incomplete closure of posterior spinal column but it does not result in any symptoms

326
Q

What is spina bifida cystica

A

Cystic formation overlying the defect on the spinal column

327
Q

What are the 3 types of spina bifida cystica

A

Meningocele
Lipomeningocele
Myelomeningeocele

328
Q

Meningocele

A

Herniation of meninges but no neurons

329
Q

Lipomeningocele

A

Herniation of meninges and fat, but no neurons

330
Q

Myelomeningeocele

A

Herniation of meninges, fat AND neuronal matter

331
Q

What is the most serious form of spina bifida

A

myelomeningeocele

332
Q

What causes cognitive deficits in spina bifida

A

Interruption in the flow and circulation of CSF

333
Q

Genetic link of spina bifida

A

Over 200 genes have been implicated but causal factors still unknown

334
Q

Environmental risk factors of spina bifida (3)

A
  1. Increased intrauterine temperature (fever)
  2. Medications
  3. Diet
335
Q

What diet deficiency is related to spina bifida

A

Folate (Vitamin B9)

336
Q

What medication is associated with spinabifida

A

Antiepileptics such as Valproic Acid

337
Q

What developmental process is folic acid necessary for?

A

Myelination –> turning off genes at the proper time

338
Q

Valproic acid increased what NT? What effect can affect can this have on the nervous system?

A

Increases GABA

Might inhibit movement which would impact the activity dependent mechanisms in the NS

339
Q

The defect is usually seen at what two levels in the spinal cord with spina bifida. What can this cause?

A

Thoracic and lumo-sacral

Can cause chronic pain

340
Q

There are usually _____ and ____ deficits below the defect in spina bifida

A

motor and sensory

341
Q

4 Other common physical features of spina bifida

A
  • Bowel and bladder issues
  • Orthopedic complications
  • Sleep disordered breathing
  • Latex allergy
342
Q

Hydrocephalus is commin in spina bifida. What can this affect?

A

Visual-perceotual and motor functioning

343
Q

What imaging tests are done to screen for spina bifida

A

Ultrasound, and then an MRI to confirm

344
Q

What is often seen on an MRI of people with spina bifida

A

Agenesis of the corpus callosum = premature degeneration

345
Q

What is done to treat the hydrocephaly in spina bifida

A

A shunt in installed to drain the excess fluid

346
Q

Seizure

A

Abnormal brain activity

347
Q

What percentage of people who have experienced a seizure develop epilepsy?

348
Q

Epilepsy

A

Recurrent disturbances in electrical activity in the brain resulting in seizures

349
Q

Why are seizures more common in children under 5

A

Because the immature brain is more excitable

350
Q

What is the hypothetical link between microglia and seizures? (3)

A

Results in:

  • increased neuronal excitability
  • decreased trophic factors
  • altered synaptic pruning
351
Q

Mutations in _______ gives you a higher vulnerability for seizures

A

voltage gated sodium channels

352
Q

What is the gene that gets mutated that results in abnormal voltage gated sodium channels

A

Sodium channel, Voltage-gated type 1-A (SCN1A)

353
Q

What type of mutation caused the SCN1A mutation in epilepsy

A

Missense mutation

354
Q

There are reduced sodium channels in what type of neuron? This leads to what?

A

GABAergic interneuron

Results in decreased inhibition

355
Q

Environmental factors that are known to induce seizures (3)

A
  • Fever
  • Increased stress/excitation
  • Prone to anxiety
356
Q

Even though there aren’t structural abnormalities with epilepsy, there are often what abnormalities

A

Functional

357
Q

What is used to detect functional abnormalities in epilepsy

358
Q

Classification of seizures (3)

A
  1. Symptomatic (known environmental trigger)
  2. Cryptogenic (cause undetermined cause, but related to other cognitive condition)
  3. Idiopathic
359
Q

Progressive unilateral encephalopathy

A

A totally healthy person suddenly has a seizure of no known cause

360
Q

Brain function abnormalities in epilepsy

A

Often deficiencies in executive function and motor abnormalities

361
Q

What are the 2 anti-convulsants often used to treat epilepsy and how do they work?

A
  1. Clonazepam (benzodiazepine) - binds to GABA neuron and induces inhibition
  2. Valproic Acid (blocks sodium channels)
362
Q

Seizure activity can increase what NT

363
Q

More BDNF does what to synapses?

A

Causes more synapses to be formed and thus allows for more excitability

364
Q

Why can too much BDNF be bad?

A

It increase excitatory synaptic connections which can cause hyper excitation in the brain and result in a seizure

365
Q

Retts syndrome is part of what spectrum of disordeers?

A

Autism spectrum

366
Q

What is the most common cause of mental retardation in females

A

Retts syndrome

367
Q

What is the typical course of development in someone with Retts

A

they will develop normally in infancy and normal childhood and then there will be a significant developmental degeneration

368
Q

Classical or Typical Retts

A

Symptoms emerge between 6-18 months of age

369
Q

Atypical Retts

A

Symptoms appear early (soon after birth) or late (after 18 month-4 years old)

370
Q

Retts is most common in females, can makes have this disorder?

A

Yes but they often die soon after birth

371
Q

What is the symptomology pattern in people with atypical Retts

A

Heterogeneous (individual variation) and the symptoms are less severe

372
Q

Pre-stage 1 Retts

A

Normal early development

373
Q

Stage 1 Retts: Early onset stagnation

A

6-18 months

Only see stereotyped hand movements and loss of interest

374
Q

Stage 2 Retts: Rapid destructive

A

18months

Language and motor deterioration

375
Q

Stage 3 Retts: Plateau

A

1-10 years

Breaking, sleep and motor abnormalities

376
Q

Stage 4 Retts: Late motor deterioration

A

Motor and intellectual disabilities

377
Q

Retts is linked to mutations in what gene?

378
Q

What chromosome is MECP2 on?

A

X chromosome

379
Q

What does the MECP2 gene do?

A

It is a member of the methyl-binding protein family that silences genes to regulate transcription

380
Q

Where is the MECP2 gene expressed

A

In the brain and other tissues

381
Q

There is increased expression of MECP2 as we age?

A

In the cortex

382
Q

What is MECP2 thought to be integral for because it increases in the cortex with age?

A

Regulating and maintaining the state of the nervous system

383
Q

In Rett syndrome, a mutation to the MECP2 gene results in what for the protein?

A

Reduced or eliminated function of the MECP2 protein function

384
Q

What does a lack of MECP2 protein function impair normal neurodevelopment?

A

Because many genes stay turned ON at inappropriate times during development

385
Q

Percentage of Retts associated with a:

  1. missense mutation
  2. Nonsense mutation
  3. C-terminal deletion
  4. Large deletion
A
  1. 39%
  2. 35%
  3. 8.7%
  4. 6.4%
386
Q

Frame shift mutation

A

When a nucleotide is deleted or inserted that results in a DIFFERENt amino acid at the point o f mutation that results in a STOP codon

387
Q

Nonsense mutation

A

Single nucleotide polymorphism (switch) which leads to a STOP codon
»Still have same # amino acids

388
Q

Mis-sense mutation

A

A single nucleotide polymorphism (switch) that results in a different amino acid being produced, but does not affect sequence or length f protein

389
Q

What is the issue with producing a premature stop codon?

A

The protein does not get fully formed and is shorter

390
Q

What is the problem with having a different amino acid?

A

Can affect protein folding

391
Q

All mutations can affect __________ with can change how the protein will eventually function

A

Post translational modification

392
Q

There are less severe symptoms of Retts when:

A

the mutation allows the protein to be longer so the protein does not lose all function

393
Q

Missense mutation T158M in Retts

A

Threonine 158 converted to methionine

394
Q

A T158M knock-in animal model provided evidence for what?

A

A causal roll of MECP2 mutation in the development of Retts like symptoms

395
Q

What symptoms did the T158M animal model for Retts show? (3)

A
  • Developmental regression
  • Motor dysfunction
  • Learning and memory deficits
396
Q

MECP2 regulates what NT, what affect does this have on development

A

BDNF

Imacts neuroplasticity

397
Q

MECP2 also regulates the production of what kinase?

A

Cyclin dependent kinase 5 (cdk5)

398
Q

MECP2 _______ cdk5 expression when normally functioning

399
Q

What is CDK5 vital for during neurdevelopment

A

Layering pattern of the cortex

400
Q

What white matter tract is 30% smaller in people with Retts

A

Corpus callosum

401
Q

There is an overall _____ in white and grey matter in Retts

402
Q

There are small neurons in what 5 brain regions in Retts

A 
Cerebral cortex 
thalamus 
basal ganglia 
amygdala 
hippocampus
403
Q

There is an overall ____ in the number of synapses in Retts

404
Q

There are low levels of what 3 NT monoamine in Retts syndrome

A

Dopamine
Serotonin
Norepinephrine

405
Q

What is theMonoamine Hypothesis of RTT

A

Early lesions in the midbrain and brainstem areas lead to inadequate synaptogenesis

406
Q

The lack of regulation by MECP2 leads to higher levels of glutamate in Retts which results in what?

A

Hyperexcitability of vast numbers of neurons in the brain

407
Q

Can Retts be cured?

408
Q

What is the structure of the mitochondria

A

Tube shapes with double membranes, there is an inner-membrane space and mitochondrial matrix

409
Q

mtDNA stands for

A

mitochondrial DNA

410
Q

What is the mitochondria essential for?

A

Producing energy for the energy hungry neurons

411
Q

Cristae

A

Folds of the inner membrane of the mitcho

412
Q

Matrix

A

Inside inner membrane of mitcho

413
Q

Intermembrane space

A

space beteen mambranes of mitcho

414
Q

What things are located in the inner membrane

A

Mitochondria DNA and electron transport chain

415
Q

Which parent are mitochondria inherited from?

416
Q

Why is there a high rate of mutation in mitcho DNA

A

Because it does not have effective repair mechanisms

417
Q

What are the symptoms of mitochondrial DNA disorders?

A

High variability because there are many different types of mutations

418
Q

How can mutations in the nuclear DNA affect mitochondrial function?

A

Proteins made by the nuclear DNA are used in the mitochondria

419
Q

Mitochondrial myophathy is a common mitochondrial disorder, what is it characterized by?

A

significant neuromuscular abnormalities

420
Q

What is Leigh Disease caused by and what does it affect

A

30 mutations in mtDNA

|&raquo_space;>Affects Cytochrome C Oxidase (COX)

421
Q

What is Cytochrome C Oxidase

A

Complex 4 of the electron transport chain

422
Q

Why is the mitochondria often affected by oxidative stres?

A

It deals with a lot of oxygen to ROS can build up and kill the cells

423
Q

What is retrograde communication

A

Pathway of communication from the mitochondria to the nucleus

424
Q

How can a dysfunctioning mitochondria alter the expression of proteins in a cell

A

Mitochondria will not produce enough energy so it will send signals to the nucleus to stop producing so many proteins to conserve energy

425
Q

What ion does the mitochondria heavily regulate? If the mitcho is not regulating it properly, what is affected?

A

Calcium

It will affect the neurons ability to communicate

426
Q

When mitochondrias are not working properly what cells are most affected?

A

Cells that require a lot of energy like neurons and muscle cells

427
Q

Leigh disease is a subtype of Subacute Necrotizing Encephalomyelopathy. Ways does that mean

A 
Subacute = rapic onset of symptoms 
Necrotizing = irreversable neuron death 
Encephalomyelo = nervous system: brain and spinal cord
428
Q

When complex 1 is not functioning in mitochondria it cannot produce energy. What does this result in?

A

A starvation of the neurons where they cannot function

429
Q

Mitochondrial dysfunction contributes to what type of cell death the most. What disease is it correlated with

A

Dopaminergic cells

Parkinsons

430
Q

MPTP is taken up by what types of cells?

A

Dopamine cells

431
Q

What does MPTP do when it is taken u pby dopamine cells?

A

Inhibits complex 1 of the electron transport chain, which starves the cells and kills them

432
Q

The loss of dopamine neurons caused by MPTP kill what brain structure and results in what type of symptoms

A

Kills neurons in the substantia nigra and causes Parkinson like symptoms

433
Q

Retrograde communication of the mitochondria with the nucleus can cause what types of epigenetic changes

A

Influences DNA methylation patterns

434
Q

Any abnormalities in complex 1 and complex 4 in the mitochondria can result in the production of what whoch causes neurodegeneration of neurons

A

Reactive oxygen species

435
Q

What are the neuroactive drugs in cannabis

A

THC and cannabidiol (CBD)

436
Q

THC binds to what receptors in the brain

A

cannabinoid receptors

437
Q

When THC binds to the cannabinoid receptors in the brain, what does it do?

A

Mimics the effects of endogeneous cannabinoids (endocannabinoids)

438
Q

What are the two main endocannabinoids in the brain?

A

Anandamine (AEA)

2-AG

439
Q

Endocannabinoids are lipophilic, what does that mean for transport?

A

Can cross the BBB and placental barrier

440
Q

What are the 2 major G-protein coupled receptors in the brain?

A

CB1-R

CB2-R

441
Q

Which of the 2 cannabinoid receptors are found most in the brain

442
Q

Where is anandemide produced?

A

In the post-synatic cell

443
Q

Where is the CB1 receptor located and stimulated?

A

On the pre-synaptic cells

444
Q

Endocanabinoids use neuomodulatory signalling, what does that mean

A

Anandemide is produced in the post-synaptic cell, and then is sent to the presynaptic cell to stimulate the CB1 receptors and regulate pre-synaptic neurotransmission

445
Q

What NT will be affected by endocannabinoids?

446
Q

What is the effect of endocannabinoids affecting the release of many NT

A

It will effect global NT homeostasis in the brain

447
Q

What receptor does THC stimulate?

448
Q

How is neurotransmission affected when THC stimulates that CB1 receptor

A

CB1 activation results in inhibition of calcium mediated vesicular neurotransmitter release

Has global impact because the CB1 receptor regulates the release of many NT

449
Q

CB1 activation can inhibit calcium influx or efflux

450
Q

What stages can cannibis affect neurodevelopment?

A

Any stage,

451
Q

What do the effects of cannabis exposure on neurodevelopment depend on?

A
  • Timing/age of exposure
  • duration of exposure
  • Dosage of exposure
  • Route of administration
452
Q

The _______ brain is vulnerable to the compounds present in cannibis

453
Q

How long can the metabolites of cannabis be detected after exposure

A

weeks after

454
Q

Both neuro____ and neuro______ effects of TCH and CBD have been observed in vitro

A

neuroprotective and neurotoxic

455
Q

The neurotoxic and neuroprotective effects of cannibis have been dseen in what cell types (2)

A

Cortical and hippocampal

456
Q

There is more significant neurotoxic effects of cannabis in the hippocampus and cortex for what age groups

A

Adolescents

457
Q

The espression pattern of CB1 receptors in the developing brain suggest a role in whay two processes?

A
  1. Axonal migration

2. Synaptogenesis

458
Q

Endocannabinoids may also play a role in regulating the survival of what cells during neurodevelopment

A

Neural progenitor cells

459
Q

Over stimulation of the CB1 receptor can have what effect on a developong btain?

A

Can throw off the normal developmental trajectory

460
Q

Prenatal exposure to cannabis has been potentially linked to what 3 types of disorders?

A
  1. Spina bifida
  2. Cognitive deficits
  3. Motor deficits
461
Q

Why is cannibis more able to get into the fetal brain?

A

The immaturity of the BBB may facilitate transportation

462
Q

Adolescent cannabis use has been observed to result in what structural abnormality

A

Lower proportion of gray matter relative to whole brain volume

463
Q

What critical process is happening in adolescent brains that may be disrupted with the use of cannabis (3)

A

The maturation of the PFC
Myelination
Synaptic pruning

464
Q

Cannabis use can mimic the symptoms of what psychiatric disorder

A

schizophrenia

465
Q

Increased expression of CB1 receptors and endocannabinoids has been observed in the braons of ______ patients

A

schizophrenia

466
Q

Marijuana use prior to the age of ____ is associated with greater risk of schizophrenia by 18

467
Q

Pluripotent cells

A

embryonic cells that can develop into any type of cell

468
Q

Multipotent cell

A

Embryonic cells that can differentiate into a few types of cells

469
Q

Neural stem cells

A

Embryonic cells that can differentiate into either neuron or glial cells

470
Q

Induced pluripotent stem cells

A

Taking an adult cell an using a chemical cocktail of transcription factors to revert adult stem cells into pluripotent cells

471
Q

What can induced pluripotent stem cells be used for?

A

Developing cell-based therapies and can also be used as a model and study disease mechanisms

472
Q

What disorder is induced pluripotent stem cells especially useful for studying?

A

Down syndrome because there are no good animal models

Can can be used to study the different types fo DS

473
Q

If a mother exercises while pregnant there has been seen to be an increase in what NT what can result in a more “,=mature” brain at 18 months

Neurodevelopmental Determents MH (2 decks)

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