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intro to psychobio > development and degeneration - week 11 > Flashcards

development and degeneration - week 11 Flashcards

1
Q

brain development
formation of the nervous system

first step

A

cell proliferation
- forms embryo
- cells can differentiate into different layers
- eventally one of these layers = neural plate

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2
Q

brain development
formation of the nervous system

2nd step

A

neurulation

neural plate folds –> neural tube

neural tube –> CNS
posterior forms spinal cord
anterior forms brain

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3
Q

what cells are neurons born from

A

progenitor cells

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4
Q

brain development

proliferation

A

progenitor cells divide asymmetrically
1 neuron and 1 progenertor cell

at the end of neurogenesis cells divide into two neurons

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5
Q

brain development

A

anterior end has swellings (known as vesicles)

each of these 5 vesicles form a predicitable region of the brain

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6
Q

error?

A

any error likely to have profound effects

MAM model of schizophrenia in rats

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7
Q

brain development

neural migration

A

neurons move and group together

specific neuroanatomy
- 6 layered cortex constructed in an inside out sequence

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8
Q

cerebral cortex

A

early generated neurons for deep cortical layers are bypassed by later born neurons that migrate to more superfivial layers

dev of cc progresses with successive waves of neuronal migration

this positions neurons within the different layers of the cortical plate

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9
Q

brain dev.

differentiation

A

newly born neurons change

not all neurons the same

generates large diversity of functionally specified neurons

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10
Q

what ensures specific neuroanatomy and specification

A

migration and differentation

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11
Q

brain dev.

neurons connect

A

migrating neurons dont have long axonal processes
axons need to form
- axonal growth

extent to target regions
- difficult to replicate in adulthood
- spinal injury

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12
Q

brain dev.

synaptogenesis

A

formation of synapses

rapid and explose in 1st 2 years after birth

issues with synapse formation –> autism and ADHD

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13
Q

brain dev.

neuronal and circuits refinement

A

only about 50% of neurons end up becoming part of brain

rest are intentially linked

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14
Q

brain dev.

neuronal and circuits refinement
- apoptosis

A

programmed cell death

eliminates defective / excessive

continues after birth

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15
Q

brain dev.

neuronal and circuits refinement
- synaptic pruning

A

enables neuronal connectivity and shaping functional wiring of brain during development

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16
Q

brain dev.

neuronal and circuits refinement
- is it automatic?

A

yes

early in life

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17
Q

brain dev.

neuronal and circuits refinement
- critical period?

A

when connectivity happens due to sensory experience

  • visual dev.
  • visual cliff experiment - depth perception
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18
Q

brain dev.

myelination

A

final process

provides both structural and metabolic support
the ensheathing of the axons by the spiral wrapping of the membrananous processes of obligodenrocytes

estimated to not complete until teenage years

underlies microstructural masturation of white matter pathways

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19
Q

brain dev.

stages

A

proliferation

neuralation

migration

differentiation

axonal growth (neurons connect)

synaptogenesis

refinement

myelination

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20
Q

neural degneration

A

refers to any pathological conditions affecting loss of neurons

a progressive deteriation of structural and functional integrity of neurons

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21
Q

neural degneration

occurs?

A

neurotraumatic

neurodegenerative

neuropsychiatric

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22
Q

neural degneration

neurotraumatic

A

sudden lack of o2

alteration in ion homeostasis

quick drop in key metabolites (AT, Glucose)

minutes - hours

eg. stroke

unspecific
- depends on place of injury

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23
Q

neural degneration

neurodegenerative

A

gradual accumalation of pathological changes

takes longer

many years

specific populations of neurons

parkinsons, alzhemers, huntingtons

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24
Q

neural degneration

age related

A

normal

multiple parts of brain

repeated concussions

brain often gets smaller due to unspecific atrophy caused by neural loss
- fewer neurons, takes up less space therefore smaller

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25
Q

neural degneration

loss of synaptic connections

A

axons degenerate

less white matter
- because no point in maintaining non functional connections

therefore smaller brain

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26
Q

2 progesses that cause neural death

A

apoptosis

necrosis

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27
Q

what causes neural death?

A

genetic

environmental

or combination

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28
Q

what causes neural death?

hyproxia

A

lack of o2

cant generate enough energy

neurons die

strokes

transient ischemic attacks

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29
Q

what causes neural death?

excessive activity

A

excitotoxic lesions in rodents

glutamate hypothesis in epilepsy

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30
Q

what causes neural death?

idiopathic / sporadic

A

disease with no identifiable cause/
/
occurring at irregular intervals or only in a few places; scattered or isolated.

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31
Q

what causes neural death?

neuronal dysfunction

A

protien aggregations

cause apoptosis

not beneficial

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32
Q

what causes neural death?

monogenetic (huntingtons)

A

mutation in a single gene

‘simpler than other neurodegernative disorders

mutation in huntington gene

inital degradation in basal ganglia

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33
Q

functional effects of loss related to…

A

site of loss

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34
Q

extent of neurodegeneration differs because

A

depends on circumstances

eg. how long brain is starved of o2

35
Q

repair and recovery

A

varies in nervous system

peripheral cells can regenerate

limited / absent in CNS
- spinal injury
- brain injury / degeneration

36
Q

repair and recovery

why not ?

A

axon regrowth not possible
following injury axons deteriorate
the ones that dont deteriorate become dysfunctional due to their loss of insulating myelin

cellular debris and bleeding results in a fluid filled cavity/cyst filling space where neurons and axons used to be

glial cells proliferate abnormally
- forming clusters of glial scars

together cysts and scars create a barrier to axons
- so prevent regrowth

37
Q

repair and recovery

why not in CNS

A

complexity of connections

connections in adulthood not the same as developing brain,, comapred to the stable connects in PNS
- synaptic plasticity over many years
- therefore functional recovery difficult as no way to reconnect and restore all the function
- where PNS based on simple connections and basic anatomy

potenially possible in spinal cord

38
Q

repair and recovery

replacing dead neurons?

A

reconnecting neurons only helps so much

neurons whose cell bodies have died cannot reconnect

39
Q

repair and recovery

generation of new neurons

A

adult neurogenesis

in some areas of brain (adult) neurons continue to proliferate

eg. dentate gyrus of hippocampus

40
Q

repair and recovery

neurogenesis for brain recovery?

A

from animal studies

new neurons are functional
- eg. in hippocampus

they differentaiate
they migrate
they form connections
they are myelinated

but if able to stimulate neurogenesis or introduce stem cells
- will correct / usefull connection be made?
- might rebuild better capactity for relearning and behavioural recovery
- unlikely to recover lost memory or skills

41
Q

repair and recovery

what does potential for recovery depend on

A

where in the nervous system the damage is

42
Q

parkinsons disease

features - motor function

A

tremor
rigid muscles
brodykinsea
hypokinsea
initally unilateral
v. early symptoms in facial expressions

43
Q

parkinsons disease

features - non motor function

A

cognitive and emotional effects

2ndary as triggered by a loss in motor function
but not just a consequence of being aware of movement problems, can characterise a general slowing of brain function

explained as a general loss of brain function

sleep deficits
depression
related to pathological processes that cause it

44
Q

parkinsons disease

causes

A

thought not to be a single condition but several underlying

45
Q

parkinsons disease

causes - idiopathic

A

no identifiable cause
most common

combination of lifestyle factors and old age

46
Q

parkinsons disease

causes - drug induced

A

slightly different from normal PD
can be caused by anti-psycotic medication
drug would need to have strong affect on the dopaminergic system
–> particularly blocking action of dopamine

features differ
- tremor, slow movement but dont progress into more severe symptoms
- clearly triggered by medication
most patients recover in months/weeks/days after stopping drug

47
Q

parkinsons disease

causes - genetic

A

less than 5% of cases
inherited
mutation s
increase likelihood
early onset disease (under 40)
only for a small minority genetic links

48
Q

parkinsons disease

causes - enviromental

A

factors can increase risk

presticides, heavy metal
infection (influenza)
alcohol / caffine?

49
Q

parkinsons disease

degeneration - substantia nigra pars compacta (SNpc)

A

all patient exhibit loss
region of midbrain

this nucleus is a component of the basal ganglia
- a group a interconnected structures found in various parts of brain
- mediates a viarity of functions (including contrubuting to motor control)
- neruons of SNpc appear darker because they contain the pigment melanin
—> byproduct of synthesis of neurotransmitter dopamine
—> dopamine is a catecholamine neurotransmitter

50
Q

parkinsons disease

degeneration - lewy bodies

A

gradual accumalation of cellular inclusions lnown as lewy bodies
—> composed of aggregates of a no. of protiens (incl. alpha-synuclein)

51
Q

parkinsons disease

degeneration - SNpc and lewy bodies

A

progressive accumulation of lewy bodies throughout the brain and loss of dopaminergic neurons ultimately results in the signs and symptoms that form basis of an initial pre mortem diagnosis of PD

52
Q

parkinsons disease

degeneration - how much loss until behavioural changes

A

evidence suggests behavioural changes not seen until 80% lf nigral dopamine is lost

53
Q

parkinsons disease

advances in technique

A

by labelling the dopamine transporters normally found on healthy presynaptic terminals of dopaminergic neurons can assess if indivduals show the cardinal signs of PD also has signs of degneration of nigral neuron terminals

54
Q

parkinsons disease

not just dopamine

A

other monoamines
- altered seretonin and noradrenaline

some studies suggest cholinergic transmission via basal nucleus of meynert may be affected (particulary later stages)

suggested that non-motor symptoms caused by non-dopaminergic changes

55
Q

parkinsons disease

not just SNpc

A

basal nucleus of meynet

cholinergic transmission

56
Q

parkinsons disease

drug treatment

A

aim of replacing / increasing dopamine
but dopamine isnt rapidly metabolised and doesnt cross blood brain barrier

57
Q

parkinsons disease

drug treatment - Levodopa

A

can cross blood brain barrier

dopamine precursor
effectivness diminshes as PD progresses
only effective of still dopaminergic neurons left

adverse effects

58
Q

parkinsons disease

drug treatment - dopamine agonists

A

target postsynaptic neurons so can still be effective

but eventually PD progressive degeration also leads to post synaptic degeneration
- neurons not recieving inputs will die
(secondary / transneuronal degeneration)

59
Q

parkinsons disease

treatment - cell transplantation

A

replacing lost neurons
attactive for PD as appears to be confined to distinct anatomical locations

the only suitable treatment as drugs dont work long term

60
Q

parkinsons disease

treatment - cell transplantation

stem cells

A

introduce into brain

right now not standard treatment
- unknown long term effects

61
Q

parkinsons disease

treatment - deep brain stimulation

A

aim of enhancing the function of remaining dopamine circuits

approach revisited after discovery of long term limitations of L-dopa

the stimulation delievered affects the neurons of the basal gangllia structure into which the electrode is implanted

causing a cascade of changed to the firing characteristics of the structures of the basal ganglia activity

if no longer benefitting for l-dopa this is considered

62
Q

alzheimers disease

A

most common form of dementia 5% of pop.
1:6 people over 80

63
Q

alzheimers disease

characteristics - memory

A

impairment in learning and memory 1st sign of disease
- initally poor memory for recent events
- more so than age related decline

followed by later impairment in attention, exectuative function, language and visual spatial function (including spatial navigation)

as progresses patients become worried, depressed or experience personality changes (become angry/violent)

64
Q

alzheimers disease

spatial navigation

A

although memory probs considered earliest sign in some cases spatial navigation probs are the 1st early impairment

some reseachers suggest it should ne considered a preclinical signs
(10-20 years before clinial onset)

65
Q

alzheimers disease

2 types

A

sporalic / late onset

early onset

66
Q

alzheimers disease

late onset

A

no obvious cause
most common (more than 90% of all cases)
later than 65
genetic predisosition + environmental factors contribute

67
Q

alzheimers disease

environmental factors

A

in addition to age
significant head injuries
heavy metals , fungicides, hypothermia

no single factor emeraged as a key candiate
keeping brain active can offset as loss i smore noticable

lifestyle risks - inactivity, smoking diet, low educational attainment

68
Q

alzheimers disease

early onset

A

1-2% caused by varients
less than 10% of all cases
1-2% inherited
under 40

69
Q

alzheimers disease

genetic factors

A

is associated with specific gene mutation

amyloid percursor protien (APP)

1 of the 2 presenilin genes

mutations in these genes thought to result in abnormal accumulation of beta-amyloid formations of amyloid plaques

70
Q

alzheimers disease

neurodegneration - temporal lobe

A

inital area of degeneration

71
Q

alzheimers disease

neurodegneration - what is the disease associated with

A

abnormal accumulation of beta-amyloid and tau protiens

  • forming amyloid plaques and neurofibrially tangles
  • aggregates of amyloid plaques form in extra cellular space between neurons
  • neurofibilarly tangles from inside cell bodies and inside neuntes, axons and dentrates
  • thought that plaques and tangles increase risk of degeneration

direct link not fully understood

72
Q

AD

neurofibilarly tangles from …..

A

inside cell bodies and inside neuntes, axons and dentrates

73
Q

AD

aggregates of amyloid plaques form….

A

in extra cellular space between neurons

74
Q

alzheimers disease

neurodegneration - tau accumalation

A

in temporal lobes
- entrotinal cortex and hippocampus (memory)
- damages memory parts 1st

75
Q

alzheimers disease

neurodegneration - interplay between tau and beta-amyloids accumalation?

A

level of beta-a accumulation reaches a tipping point

then rapid spread of tau happens

leading to more widespread neurodegeneration

so further cognitive decline

76
Q

alzheimers disease

neurodegneration - synaptic loss

A

corrolates with coginitve impairment

particularly effects chlolinergic and glutamatergic synpases

77
Q

alzheimers disease

neurodegneration - synaptic loss linked to…

A

learning and memory

and is the principle correlate of disease progression and cognitive impairment

78
Q

alzheimers disease

neurodegneration - synaptic loss where?

A

loss of cholinergic neurons in basal buccal of meyert and other subcortical structures shown to contribute to memory and attention deficits in AD

79
Q

alzheimers disease

neurodegneration - unanswered qs

A

know that amyloid plaques affect cellular function of neurons including synaptic activity (synaptic loss)

but many studies failed to find corrolation between levels of amyloid plaques and cognitive impairment

80
Q

alzheimers disease

treatment - successful? why?

A

currently no successful interventions which can prevent pprogression of AD

due to complexity of AD unlikely one drug can treat it

current approaches focus on helping patients to manage and maintain mental function and slow down memory loss

81
Q

alzheimers disease

drug treatment

A

inital aim of boosting cholinergic transmission (acetylcholine)

prolong presence of remaing acetylcholine in synapse

acetylcholinestease inhibitors
- prevent breakdown of Ach or niotinic agonists
—-> continues to stimulate receptors (minics actions)

not very effective –> helps to reduce cognitive symptoms
- dont change underlying disease progression
only help for limited time

82
Q

alzheimers disease

treatment - nicotine patches

A

smoking seems to incease risk of dementia

but some studies suggest that nicotine patches could improve memory in early stages of AD

83
Q

alzheimers disease

treatment - targeting pathology

A

pathological modification

divert Amyloid percurosor protein away from amlyoid
antibodies away from amyloid
not v. effective
is amyloid actually causal for AD ??

treatments targeting pathology aim to reduce the existing deposits or further accumulation of beta amyloid / tau proteins
- inclused beta-amyloid directed immotherapy using antibodies targeting these proteins and inhibitors taget APP
- lots of side effects

intro to psychobio (11 decks)

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