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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
types of degeneration?
- neurotraumatic diseases - neurodegenerative diseases - neuropsychiatric diseases
26
fast degeneration
occurs when a lack of key metabolites result in energy starvation and neuronal death
27
slow degeneration
occurs with 'normal' age-related decline as brains are affected by neuronal loss
28
how do brains get smalller with degeneration?
1. death of neurones means they take up less space 2. loss of synaptic connections results in less white matter
29
causes of degeneration
- hypoxia - excessive activity - idiopathic - monogenetic - neuronal dysfunction and protein aggregations
30
hypoxia
insufficient oxygen results in energy starvation and neuronal death
31
excessive activity
excitotoxic lesions and damage leads to neuronal death
32
idiopathic
neurodegeneration has an unknown mechanism
33
monogenetic
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
neuronal dysfunction and protein aggregations
causes the neurone to undergo necrosis and unbeneficial apoptosis
35
how can the peripheral nervous system regenerate?
neural damage can be repaired and function can be recovered, as long as axons re-connect to the same sensory cell or muscle
36
why is there limited repair and recovery in the CNS?
axonal regrowth is not possible in the spinal cord
37
paraplegia
loss of sensation in the legs
38
quadriplegia
loss of sensation in all four limbs
39
process of axons following injury
axons degenerate some remain intact, but become dysfunctional due to loss of insulating myelin
40
what results in a fluid-filled cavity?
cellular debris and bleeding, and these take up the space of neurones and axons
41
what creates clusters of glial cells at the cavity site?
abnormal proliferation of glial cells
42
what do the fluid-filled cavity and glial scars act as?
a barrier to axons, and prevent regrowth and re-connection
43
why is it difficult to recover from adult brain injury?
due to its complex structure and functional organisation (inter-individual differences in the brain) compared to the peripheral nervous system
44
evidence of adult neurogenesis
neural progenitor cells in the hippocampus can proliferate and differentiate to other neurones, but the role of this is unclear
45
what does adult neurogenesis indicate?
adult brain plasticity, and is involved in learning and memory
46
evidence of adult neurogenesis being involved in learning and memory
hippocampal neurogenesis levels are associated with cognitive status neurogenesis is significantly lower in patients with MCI and AD
47
what percent of the population does PD affect?
2-3% over 65-years-old
48
main types of PD
1. idiopathic parkinson's disease 2. drug-induced parkinsonism 3. genetic
49
idiopathic parkinson's disease
the most common, with no identifiable cause
50
drug-induced parkinsonism
can be caused by anti-psychotic medication symptoms do not increase in severity and recovery is possible
51
genetic PD
makes up less than 5% of cases, and is associated with early-onset disease
52
motor symptoms of PD
- tremor - rigid muscles - slowness (bradykinesia) or absence (hypokinesia) of movement - becomes bilateral upon progression - early symptoms seen in changes of facial expression
53
nonmotor symptoms of PD
- cognitive effects - emotional effects - not just a consequence of being aware of movement problems - general 'slowing' of brain function
54
how does neural degeneration occur in PD?
the loss of dopaminergic neurones results in depigmentation of the substantia nigra (specifically within the pars compacta) and PD symptoms
55
how does MPTP induce parkinsonism?
MPTP is metabolised into neurotoxic MPP+ which kills dopamine neurones due to apoptosis
56
when do mild symptoms of PD appear?
around 80% loss of dopaminergic neurones, making early diagnosis and treatment difficult
57
how can PET scans measure dopamine transporter activity?
by quantifying uptake of radioactive dopamine can detect early dopamine depletion, as low levels of dopamine will result in reduced uptake
58
which other neurotransmitters are involved in PD symptoms?
monoamines such as serotonin (5-HT) and noradrenaline
59
which other brain areas are affected by neural degeneration?
the basal nucleus of maynert is involved in cholinergic transmission into cortical areas
60
what do drug treatments for PD focus on?
substituting dopamine loss via dopamine precursor levodopa (L-DOPA)
61
why are dopamine injections ineffective?
dopamine is quickly metabolised and cannot cross the blood brain barrier
62
why is L-DOPA a better option?
L-DOPA can cross the blood brain barrier and convert neurones into dopamine but this is only effective when dopamine neuroens are present
63
function of dopamine agonists
target postsynaptic dopamine receptors, making them effective in the absence of presynaptic dopamine neuroens
64
limitations of dopamine agonists
PD will result in degeneration of postsynaptic neurones and cell death, making this ineffective
65
cell transplantation
aims to replace dopamine neurones via stem cells
66
deep brain stimulation
enhances function of dopaminergic neurones by implanting electrodes these modulate dysfunctional activity and control symptoms, but does not stop progression
67
what percent of the population does AD affect?
5%, and 1:6 over 80-years-old
68
memory symptoms of AD
- initial poor memory for recent events - more so than age-related memory decline
69
other symptoms of AD
- deficits in spatial navigation, executive function, and language - changes in personality - aggression and apathy - depressive symptoms
70
what is a sufficient causal factor of AD?
MCI
71
when is sporadic AD most common?
in late-onset, accounting for 90% of cases
72
which genetic variant increases risk of AD?
apolipoprotein gene E (APOE4)
73
what percent of cases are early onset AD?
only 10%
74
what percent of early onset AD are familial?
1-2% of these are familial and caused by mutations in APP, PSEN1 and PSEN2 these result in abnormal formation of amyloid plaques
75
how does neural degeneration occur in AD?
abnormal accumulation of beta-amyloid and tau proteins results in amyloid plaques and neurofibrillary tangles these increase the risk of neural degeneration
76
amyloid plaques
form in extra-cellular space between neurones and impair synaptic activity, resulting in synaptic loss
77
neurofibrillary tangles
form inside the cell body, neurites, axons, and dendrites
78
current treatments of AD aim to...
help patients maintain mental function, manage behavioural symptoms, and slow down memory loss
79
how can drug medication maintain cognitive function in AZ?
by boosting cholinergic transmission and prolonging the presence of acetylcholine in the synapse
80
what do pathology treatments attempt to do?
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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