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LC INTRODUCTION TO PSYCHOBIOLOGY > Development and Degeneration > Flashcards

Development and Degeneration Flashcards

1
Q

what are the stages of brain development?

A
  1. neurulation
  2. neurogenesis
  3. neuronal migration
  4. differentiation
  5. axonal regrowth and synaptogenesis
  6. connectivity refinement
  7. myelination
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2
Q

what does development begin as?

A

a single diploid cell with two chromosome cells (zygote)

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3
Q

what does zygote undergo?

A

multiple cell divisions which differentiate into different layers

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4
Q

what does one of these layers form?

A

a neural plate

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5
Q

how does the neural plate create the CNS?

A
  1. the edges of a neural plate elevate to form neural folds
  2. neural folds curve to form a U-shaped neural groove
  3. neural groove closes to form neural tube
  4. the neural tube becomes the CNS
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6
Q

what do some cells within the neural tube differentiate into?

A

neural progenitor cells

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7
Q

what do neural progenitor cells divide into?

A

one progenitor cell and one neurone

they can also give rise to glial cells

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8
Q

what is this rapid cell division and neuronal birth known as?

A

proliferation and neurogenesis

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9
Q

what occurs at the end of neurogenesis?

A

progenitor cells deplete by dividing into two neurones

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10
Q

what can disruption of proliferation result in?

A

neurodevelopmental disorders

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11
Q

where do neurones move to at the end of neurogenesis?

A

different parts of the brain, leading to the formation of the cerebral cortex

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12
Q

how is the cerebral cortex constructed?

A

six-layers, by an inside-outside sequence

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13
Q

inside-outside sequence

A

early generated neurones form deep cortical layers, and later-born neurones migrate to superficial layers (neuronal migration)

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14
Q

what occurs when newly generated neurones migrate to their final locations?

A

differentiate- make specific connections and specialised functions

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15
Q

what does migration and differentiation ensure?

A

specific neuroanatomy and brain function

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16
Q

what can be developed once neurones have reached their final destination?

A

a typical cell structure, and they can establish connectivity

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17
Q

what does connectivity require?

A

long axonal processes and formation of synapses

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18
Q

what can be caused by issues with synapse formation?

A

neurodevelopmental disorders such as autism and ADHD

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19
Q

why are 50% of neurones killed as part of the developmental process?

A

to refine the neural circuits

this occurs through apoptosis and synaptic pruning

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20
Q

apoptosis and synaptic pruning

A

eliminate defective or excessive cells

shape the functional wiring of the brain

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21
Q

how is myelin produced?

A

by oligodendrocytes (a type of glial cell) that provide structual and metabolic support, including axonal myelination

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22
Q

what does myelination facilitate?

A

nerve impulse conduction, and communication across neuronal circuits

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23
Q

neurodegeneration is…

A

a progressive deterioration of the functional and structural integrity of neurones

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24
Q

what processes underlie neuronal loss?

A

apoptosis and necrosis

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25
Q

types of degeneration?

A
  • neurotraumatic diseases
  • neurodegenerative diseases
  • neuropsychiatric diseases
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26
Q

fast degeneration

A

occurs when a lack of key metabolites result in energy starvation and neuronal death

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27
Q

slow degeneration

A

occurs with ‘normal’ age-related decline as brains are affected by neuronal loss

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28
Q

how do brains get smalller with degeneration?

A
  1. death of neurones means they take up less space
  2. loss of synaptic connections results in less white matter
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29
Q

causes of degeneration

A
  • hypoxia
  • excessive activity
  • idiopathic
  • monogenetic
  • neuronal dysfunction and protein aggregations
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30
Q

hypoxia

A

insufficient oxygen results in energy starvation and neuronal death

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31
Q

excessive activity

A

excitotoxic lesions and damage leads to neuronal death

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32
Q

idiopathic

A

neurodegeneration has an unknown mechanism

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33
Q

monogenetic

A

caused by a single gene mutation

seen in HD being attributable to inherited mutation in HTT, resulting in the fragmentation of an abnormally long huntingtin gene

34
Q

neuronal dysfunction and protein aggregations

A

causes the neurone to undergo necrosis and unbeneficial apoptosis

35
Q

how can the peripheral nervous system regenerate?

A

neural damage can be repaired and function can be recovered, as long as axons re-connect to the same sensory cell or muscle

36
Q

why is there limited repair and recovery in the CNS?

A

axonal regrowth is not possible in the spinal cord

37
Q

paraplegia

A

loss of sensation in the legs

38
Q

quadriplegia

A

loss of sensation in all four limbs

39
Q

process of axons following injury

A

axons degenerate

some remain intact, but become dysfunctional due to loss of insulating myelin

40
Q

what results in a fluid-filled cavity?

A

cellular debris and bleeding, and these take up the space of neurones and axons

41
Q

what creates clusters of glial cells at the cavity site?

A

abnormal proliferation of glial cells

42
Q

what do the fluid-filled cavity and glial scars act as?

A

a barrier to axons, and prevent regrowth and re-connection

43
Q

why is it difficult to recover from adult brain injury?

A

due to its complex structure and functional organisation (inter-individual differences in the brain) compared to the peripheral nervous system

44
Q

evidence of adult neurogenesis

A

neural progenitor cells in the hippocampus can proliferate and differentiate to other neurones, but the role of this is unclear

45
Q

what does adult neurogenesis indicate?

A

adult brain plasticity, and is involved in learning and memory

46
Q

evidence of adult neurogenesis being involved in learning and memory

A

hippocampal neurogenesis levels are associated with cognitive status

neurogenesis is significantly lower in patients with MCI and AD

47
Q

what percent of the population does PD affect?

A

2-3% over 65-years-old

48
Q

main types of PD

A
  1. idiopathic parkinson’s disease
  2. drug-induced parkinsonism
  3. genetic
49
Q

idiopathic parkinson’s disease

A

the most common, with no identifiable cause

50
Q

drug-induced parkinsonism

A

can be caused by anti-psychotic medication

symptoms do not increase in severity and recovery is possible

51
Q

genetic PD

A

makes up less than 5% of cases, and is associated with early-onset disease

52
Q

motor symptoms of PD

A
  • tremor
  • rigid muscles
  • slowness (bradykinesia) or absence (hypokinesia) of movement
  • becomes bilateral upon progression
  • early symptoms seen in changes of facial expression
53
Q

nonmotor symptoms of PD

A
  • cognitive effects
  • emotional effects
  • not just a consequence of being aware of movement problems
  • general ‘slowing’ of brain function
54
Q

how does neural degeneration occur in PD?

A

the loss of dopaminergic neurones results in depigmentation of the substantia nigra (specifically within the pars compacta) and PD symptoms

55
Q

how does MPTP induce parkinsonism?

A

MPTP is metabolised into neurotoxic MPP+ which kills dopamine neurones due to apoptosis

56
Q

when do mild symptoms of PD appear?

A

around 80% loss of dopaminergic neurones, making early diagnosis and treatment difficult

57
Q

how can PET scans measure dopamine transporter activity?

A

by quantifying uptake of radioactive dopamine

can detect early dopamine depletion, as low levels of dopamine will result in reduced uptake

58
Q

which other neurotransmitters are involved in PD symptoms?

A

monoamines such as serotonin (5-HT) and noradrenaline

59
Q

which other brain areas are affected by neural degeneration?

A

the basal nucleus of maynert is involved in cholinergic transmission into cortical areas

60
Q

what do drug treatments for PD focus on?

A

substituting dopamine loss via dopamine precursor levodopa (L-DOPA)

61
Q

why are dopamine injections ineffective?

A

dopamine is quickly metabolised and cannot cross the blood brain barrier

62
Q

why is L-DOPA a better option?

A

L-DOPA can cross the blood brain barrier and convert neurones into dopamine

but this is only effective when dopamine neuroens are present

63
Q

function of dopamine agonists

A

target postsynaptic dopamine receptors, making them effective in the absence of presynaptic dopamine neuroens

64
Q

limitations of dopamine agonists

A

PD will result in degeneration of postsynaptic neurones and cell death, making this ineffective

65
Q

cell transplantation

A

aims to replace dopamine neurones via stem cells

66
Q

deep brain stimulation

A

enhances function of dopaminergic neurones by implanting electrodes

these modulate dysfunctional activity and control symptoms, but does not stop progression

67
Q

what percent of the population does AD affect?

A

5%, and 1:6 over 80-years-old

68
Q

memory symptoms of AD

A
  • initial poor memory for recent events
  • more so than age-related memory decline
69
Q

other symptoms of AD

A
  • deficits in spatial navigation, executive function, and language
  • changes in personality
  • aggression and apathy
  • depressive symptoms
70
Q

what is a sufficient causal factor of AD?

A

MCI

71
Q

when is sporadic AD most common?

A

in late-onset, accounting for 90% of cases

72
Q

which genetic variant increases risk of AD?

A

apolipoprotein gene E (APOE4)

73
Q

what percent of cases are early onset AD?

A

only 10%

74
Q

what percent of early onset AD are familial?

A

1-2% of these are familial and caused by mutations in APP, PSEN1 and PSEN2

these result in abnormal formation of amyloid plaques

75
Q

how does neural degeneration occur in AD?

A

abnormal accumulation of beta-amyloid and tau proteins results in amyloid plaques and neurofibrillary tangles

these increase the risk of neural degeneration

76
Q

amyloid plaques

A

form in extra-cellular space between neurones and impair synaptic activity, resulting in synaptic loss

77
Q

neurofibrillary tangles

A

form inside the cell body, neurites, axons, and dendrites

78
Q

current treatments of AD aim to…

A

help patients maintain mental function, manage behavioural symptoms, and slow down memory loss

79
Q

how can drug medication maintain cognitive function in AZ?

A

by boosting cholinergic transmission and prolonging the presence of acetylcholine in the synapse

80
Q

what do pathology treatments attempt to do?

A

divert APP away from amyloid by using antibodies, but this is reliant in beta-amyloid and tau hypothesis

LC INTRODUCTION TO PSYCHOBIOLOGY (8 decks)

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