The Developing Brain

Front 1

Gastrulation

Back 1

Process in which the zygote forms clefts and the bottom folds inwards.

Front 2

Mesoderm

Back 2

Skeletal, muscular and cardiovascular systems

Front 3

Endoderm

Back 3

Urinary, digestive and respiratory systems.

Front 4

Ectoderm

Back 4

Skin- and nervous system

Front 5

Neurulation

Back 5

Part of the mesoderm forms into notochord and then in the neural tube.

Front 6

Teratogen

Back 6

Agent that causes malformations in embryos

Front 7

How are HOX-genes regulated?

Back 7

By retinoic acid produced by Hensen's node

Front 8

Features of neural stem cells

Back 8

Multipotent, unlimited capacity for cell division and self-renewing

Front 9

Where does neurogenesis take place?

Back 9

Ventricular zone (during development) and subventricular zone (throughout life)

Front 10

Radial migration

Back 10

Neurons travel via the radial glia cells to the cortical plate, new neurons on top of old neurons

Front 11

Radial migration defects

Back 11

Microcephaly, Lissencephaly, inverted cortical layering and cobblestone cortex

Front 12

What happens in Netrin knockout mice?

Back 12

Axons do not cross throughout the floorplate.

Front 13

Axon guidance

Back 13

Process during which axonal processes find their way from the neuronal cell body to target structures elsewhere in or outside the nervous system.

Front 14

Sensitive period

Back 14

A limited time during development during which the effect of experience on brain function is particalarly strong

Front 15

Critical period

Back 15

A strict time window during which experience provides information that is essential for normal development and permanently alters performance

Front 16

Criteria for intellectual disability

Back 16

Low IQ (<70), limitations in adaptive behaviours and mental manifestations began before the age of 18.

Front 17

Comorbidity between ID, autism and epilepsy

Back 17

40% of people with ID have autism, 50-85% of autism have ID and 30% of epilepsy have autism.

Front 18

Valproic Acid (VPA)

Back 18

Anti-epileptic and mood-stabilising drug, but also associated with 3 times higher chance of offspring with autism

Front 19

Synaptopathy

Back 19

abnormality of synapse structure and function underlie brain disorders, including ID

Front 20

Main hypotheses for neurodevelopmental disorders?

Back 20

Altered brain connectivity and critical period dysregulation

Front 21

Autism spectrum disorders in DSM4

Back 21

Classic autistic disorder, aspergers disorder, childhood disintergrative disorder, and catch-all diagnosis

Front 22

Autism spectrum disorders in DSM5

Back 22

Level 3 requiring very substantial support, level 2 substantial support and level 1 support (former asperger)

Front 23

Why are there more people with Asperger in IT?

Back 23

Systemizing skills required in computing. Autists are more efficient with that than language.

Front 24

Heritability and concordance for autism

Back 24

90% heritability, MZ twins concordance 90% and 10% in DZ twins.

Front 25

Critical periods for human development

Back 25

Embryonic, fetal and postnatal.

Front 26

Types of teratogens

Back 26

Infectious agents (rubella), pharmacological (thalidomide, aspirin), industrial (pesticides, mercury), recreational (alcohol, nicotine)

Front 27

What was Thalidomide?

Back 27

Drug given to mothers to prevent morning sickness in late 50s/early 60s -> children born without arms or legs

Front 28

Facial features of Fetal alcohol syndrome

Back 28

Narrow forehead, small eyes, small nose and midface, and longer upper lip without philtrum

Front 29

Effect of nicotine on fetus

Back 29

constrict blood vessels, causes placenta to grow abnormally, reduces transfer of nutrients to fetus.

Front 30

Chemo-affinity hypothesis

Back 30

Molecular coding defines synapse specificity (wiring determined by genotype), however not likely hypothesis.

Front 31

What is remarkable in fragile X syndrome

Back 31

Many spines on the dendrites stay in a immature state.

Front 32

Positive long-term effects of alcohol consumption

Back 32

lower risk for diabetis, less silent infarcts in the brain, better blood flow, higher bone mineral density, reduced risk of gallstones and kidneystones

Front 33

Negative long-term effects of high alcohol consumption

Back 33

Impaired development, pstchological disadvantages, increased risk of diabetis and cancer in mouth area

Front 34

What does alcohol do with the GABA receptor?

Back 34

It keeps the receptor longer open so normal inhibition is strengthened

Front 35

What does alcohol do with the NMDA receptor?

Back 35

It inhibits the function and acts like a pore blocker

Front 36

What has alcohol to do with the subventricular zone?

Back 36

It affects dividing neurons in the subventricular zone of the hippocampus, which are necessary for plasticity

Front 37

Why do nicotine exposed rats have attention defecits?

Back 37

A metabotic glutamate receptor is decreased in expression and function after nicotine exposure, which is involved in attention.

Front 38

Delusions

Back 38

Misinterpretation of perception or experience

Front 39

Dopamine hypothesis of Schizophrenia

Back 39

Cocaine and Amphetamine that cause more dopamine in synapse, can lead to psychosis similair to schizophrenia.

Front 40

Mesolimbic pathway in schizphrenia

Back 40

Too much dopamine in ventral striatum due to hyperactive dopamine neurons -> positive symptoms

Front 41

Mesocortical pathway in schizophrenia

Back 41

Too little dopamine in prefrontal cortex due to hypoactive dopamine neurons -> negative and cognitive symptoms

Front 42

Negative effect antypsychotic D2-antagonist in Schizophrenia

Back 42

It blocks hyperactive mesolimbic circuits and thus positive symptoms, but causes parkinsonlike side effects due to blockade nigrostriatal pathway

Front 43

Glutamate hypothesis of Schizophrenia

Back 43

NMDA-antagonists like PCP and ketamine cause temporary state of mind very similar to schizophrenia

Front 44

Why does sensory filter in schizophrenics dysfunction?

Back 44

Excess DOPA from mesolimbic pathway inhibits GABA, NMDA-r hypofunction causes less effect and less GABA in thalamus causes less filtering

Front 45

Key susceptibility genes in schizophrenia

Back 45

Dysbindin, BDNF, DISC-1 and neurogulin -> abnormal synapse formation and dendritic morphology

Front 46

Course of schizophrenia

Back 46

Premorbid, Prodromal, Progression and Residual

Front 47

Biggest brain differences in schizophrenia

Back 47

Large ventricles, less thickning in adolescence, more thinning later age, decrease in gray matter

Front 48

How do antipsychotics in schizophrenia change cortical thinkness?

Back 48

Higher cumulative typical antipsychotics (HAL) more thinning. Higher cumulative atypical (OLZ) less thinning.

Front 49

Effects of cannabis on schizophrenia

Back 49

It's highly prevalent, reduces age of onset and result in greater brain volume changes.

Front 50

What are the effects of physical exercise in schizophrenia?

Back 50

Reduction of clinical symptoms, improving physical health and attentuate the progressive brain volume changes.

Front 51

What is the default pathway when it comes to sex-determination?

Back 51

The default pathway is female, a male child will not develop unless there are androgens from testis present

Front 52

Mullerian system

Back 52

embryonic precursors of female internal sex organs

Front 53

Wolffian system

Back 53

embryonic precursors of male internal sex organs

Front 54

Which hormones are needed to make male?

Back 54

anti-mullerian hormone to inhibit development of female sex organs and androgens to develop male organs.

Front 55

Androgen insensitivity syndrome

Back 55

Caused by lack of functioning androgen receptors, will make a female with XY chromosomes but no internal sex organs.

Front 56

Persistent mullerian duct syndrome

Back 56

Caused by lack of anti-mullerian hormone or receptors. In a male this will develop both male and female internal sex organs

Front 57

Congenital androgen hyperplasia

Back 57

Boys develop normal but girls get more 'male-like' , also more likely to be lesbian/bisexual

Front 58

Concordance for homosexuality

Back 58

50% in mztwins and 20% in dz twins

Front 59

Paradox in homosexuality

Back 59

Male homosexuals have 80% fewer children, but female relatives have much higher fertility rates. Gene on X chromosome causes both.

Front 60

What can be the underlying reason for gender dysphoria?

Back 60

Sexual differentiation of genitals and sexual differentiation in brain are influenced independently and in different times.

Front 61

What is the road to treatment of young transsexuals?

Back 61

Postpone puberty with hormone-blocking drugs, then cross-sex hormones and eventually sex reassignment surgery.

Front 62

Are children gender-neutral at birth

Back 62

No, boy raised as a girl due to impaired circumcision and became gender dysphoric

Front 63

What is the difference between gender role and gender identity?

Back 63

Gender role is preference for same or other sex roles, toys, playmates etc. While gender identity is the real desire to be the other gender.

Front 64

How many GD children become GD adolescents?

Back 64

15.8%

Front 65

Symptoms of Parkinson's disease

Back 65

Motor symptoms like tremor and instability. Non-motor symptoms like cognitive impairments and sleep problems

Front 66

Biological aging

Back 66

Reaches peek around early twenties and declines slowly over time

Front 67

Social aging

Back 67

Reaches peek around late fifties, but declines fastly when retired

Front 68

Psychological age

Back 68

Increases slowly with age (except in forms of alzheimer)

Front 69

Passive aging theory (evolutionary)

Back 69

No evolutionary benefit of longer life after reproductive maturity has been reached

Front 70

Active aging theory (evolutionary)

Back 70

Some organisms limit own lifespan in order to provide diffuse evolutionary benefits to younger members

Front 71

Telomere theory (biological)

Back 71

All cells have limited capacity to replicate due to progressive shortening of chromosome's telomeres

Front 72

Cross-linkage theory (biological)

Back 72

Accumulation of cross-linked proteins interferes with normal cell function

Front 73

Free-radical theory (biological)

Back 73

Impaired mitochondria produce ROS that in turn can damage DNA, proteins and lipids

Front 74

DNA damage theory (biological)

Back 74

Stochastic accumulation of DNA damage results in cellular senescence and prevents cancer

Front 75

Caloric restriction theory (biological)

Back 75

Reducing food intake shifts energy distributioin from growth to maintenance and results in more efficient metabolism and less toxic side products

Front 76

Sirtuin theory (biological)

Back 76

Involved in the regulation of multiple cellular processes, sirtuins may prolong lifespan under conditions of cellular adaptation

Front 77

What types of biological theories of aging are there?

Back 77

genetic, non-genetic and system theories

Front 78

What may limit plasticity in aging hippocampus?

Back 78

Increased extracellular matrix levels

Front 79

Neurofibrallary tangles

Back 79

Caused by Tau protein and are intracellular included

Front 80

Neuritic plaques

Back 80

Caused by Amyloid-beta protein and are extracellular depositioned

Front 81

Memory areas

Back 81

Prefrontal cortex, hippocampus, amygdala and cerebellum

Front 82

What are great predictors for alzheimer in the brain?

Back 82

Atrophy of hippocampus and abnormal amyloid beta levels in cerebrospinal fluid

Front 83

Neurodegenerative disorders

Back 83

Marked with progressive loss of neurons, many are associated with abnormal aggregations in brain

Front 84

Which neurons die in alzheimer?

Back 84

Cholinergic neurons, glutamatergic cells, noradrenergic neurons and serotonergic neurons

Front 85

What genes are strongly associated with alzheimer?

Back 85

Amyloid precursor protein, presenilin 1 and presenilin 2

Front 86

What makes treating alzheimer so difficult?

Back 86

Treating late symptoms not effective and certainty of disease only after death (brain atopsy), only treatment of early synaptic dysfunction possible.

Front 87

Main brain pathology Alzheimer

Back 87

In temperopartial cortex, cerebral atrophy, A-beta plaques and tangles

Front 88

Main brain pathology Parkinson

Back 88

In midbrain, pallor of substantia nigra and lewy bodies

Front 89

Protoasome

Back 89

Degraded native conformation of misfolded monomer

Front 90

Autophagy

Back 90

Degraded misfolded monomer or oligomer

Front 91

Inclusion body

Back 91

Degraded oligomer or fibril

Front 92

Chaperones

Back 92

A protein quality control that recognizes and refolds

Front 93

Degradation

Back 93

Protein quality control proteasome and autophalagy

Front 94

Stress responses

Back 94

Unfolded protein response and heatshock response

Front 95

Tau

Back 95

Microtubule binding protein, stabilises microtubules and dynamic phosphorylation/dephosphorylation

Front 96

How to restore autophagy in Alzheimer

Back 96

Activation using rapamycin and overexpression TFEB

Front 97

Why does protein quality control not prevent accumulation in neurodegenerative disorders?

Back 97

Cells in brain cannot divide and simply erase aggregation. Disease is age related and thus gradually builds up.

Front 98

Exogenous DNA damage

Back 98

UV, radiation, chemicals

Front 99

Endogenous DNA damage

Back 99

ROS, alkylation

Front 100

What happens when altered DNA metabolism leads to misreplication or segregation?

Back 100

Mutations occur, which can cause cancer

Front 101

What happens when altered DNA metabolism lead to blocked transcription or blocked replication?

Back 101

Cell cycle delay or cell death, which cause aging

Front 102

Why do Xeroderma Pigmentosum lead to cancer?

Back 102

Global genome NER (everywhere, but slow) doesn't function which is needed for the prevention of mutations

Front 103

Why do Cockayne syndrome and Trichothiodystrophy lead to fast aging?

Back 103

Transcription coupled NER (fast, but specific places) doesn't function which is needed for promoting cell survival.

Front 104

How can accelerated aging be stopped?

Back 104

Dietary restriction

Front 105

Aging brain model

Back 105

Older persons positivity effect is a consequence of age-related decline in the amygdala

Front 106

Cognitive control

Back 106

Positivity effect is a result of older persons greater focus on regulating emotion

Front 107

How will older brain compensate for loss?

Back 107

Increasing frontal acitivty (PASA), more symmetry hemispheres (HAROLD), and compensation of neural circuits (CRUNCH)

Front 108

The plus side of religion in older persons?

Back 108

May buffer against hippocampal atrophy and cognitive decline

Front 109

Neural tube in embryonic development

Back 109

Originates from the ectoderm and gives rise to CNS

Front 110

How is radial growth of cortex established?

Back 110

By migration of new neurons from the ventricular zone toward outer cortical layers

Front 111

Direction of growth in developing axon

Back 111

chemo-attractive or -repulsive gradients, membrane-bound factors, and dynamic properties of actin cytoskeleton

Front 112

Why is retinoic acid important in early brain development?

Back 112

A rostro-caudal gradient of RA defines patterning along the rostro-caudal axis of neural tube

Front 113

How do developing axons cross the midline?

Back 113

By alterations in the expression of guidance receptors.

Front 114

Dynamic properties of growth cone filipodia

Back 114

Due to guidance receptors on the filipodial membrane

Front 115

What is the Rho family of signalling proteins?

Back 115

Small GTPases that regulate growth, adhesion and trafficking processes in the cell (like CDC42, RhoA and Racl)

Front 116

What is the fragile X syndrome?

Back 116

An impairment of the Fmr1 gene

Front 117

Abnormalities associated with ASD

Back 117

Abnormal number of neurons, brain growth and white matter

Front 118

What is required for topographic mapping in the retino-tectal system?

Back 118

Different levels of Ephrin expression in different layers in the tectum and receptor expression of retinal ganglion cells

Front 119

Protocadherins

Back 119

Dictating synaptic specificity, are cell-cell adhesion proteins and thousands are generated by alternative splicing

Front 120

What is abnormal in women with androgen insensitivity syndrome?

Back 120

They have testes that produce testosterone

Front 121

The extracellular matrix

Back 121

Crucial role in hippocampal synaptic plasticity and contribute to ending of the critical period

Front 122

How can caloric restriction prolong lifespan?

Back 122

By reducing mammalian target of rapamycin (mTOR) signalling

Front 123

Which genes are frequently mutated in early onset Alzheimer?

Back 123

APP and PSEN1

Front 124

Important contributors to alzheimer disease progression

Back 124

synaptic dysfunctions, microglial activation and immune responses, and brain atrophy

Front 125

How can alzheimer be found using brain imaging?

Back 125

Using a PET scan to detect fibrillary amyloid-beta deposits

Front 126

Function of DJ1 (Parkinson)

Back 126

Acts as positive regulator of androgen receptor-dependent transcription, functions as chaperone, sensor of oxidative stress, protect against cell death

Front 127

Mutation in DJ1

Back 127

L166P, transcription impairment change from leucine to proline

Front 128

Where is DJ1 expressed?

Back 128

Hippocampus

Front 129

Remarkable paradox between Dj1 expression and cause of PD?

Back 129

It is expressed everywhere, not only substantia nigra