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Ageing > Brain ageing > Flashcards

Brain ageing Flashcards

1
Q

what is synaptic plasticity ?

A

when synapses strengthen or weaken over time due to changes in activity levels

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2
Q

what are the 2 types of plasticity ?

A

local and global

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3
Q

Whats TMS?

A

transcranial magnetic stimulation - can induce changes in brain plasticity

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4
Q

what influences brain trajectories of plasticity ?

A

exposure to disease stress, genetics and diet

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5
Q

how does the structure of the brain change?

A

in responce to behavioural deficits and general decline i volume over time due to reduced synaptic activity

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6
Q

key neurotransmitter?

A

ca2+

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7
Q

where was the protosynapse found ?

A

in unicellular organisms

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8
Q

whats PSD ?

A

post synaptic density

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9
Q

3 main types of proteins ?

A

receptor, enzyme and scaffold

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10
Q

whats EPSP?

A

excitatory post synaptic potentical

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11
Q

what ca2+ affinity does camkinase 11 have ?

A

low , phosphorylates NMDA

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12
Q

what do glail cells do ?

A

regulate the levels of glutamate

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13
Q

examples of NMDA subunits?

A

GluN1&2A-D ( need at least one N1 and N2 ), sodium

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14
Q

examples of AMPA subunits?

A

GluA1-4&A2 (controls calcium, often blocked by mg2+)

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15
Q

whats LTP?

A

long term pertensiation

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16
Q

whast LTD?

A

long term depression

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17
Q

whats STP?

A

short term pertensation

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18
Q

what influences if its LTP OR LTD?

A

signal strength, timing subtypes present

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19
Q

two types of LTP?

A

early ( local at the synapses level) and late ( cause gene changes and influences other nearby synapses to activate)

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20
Q

example of a scaffold protein?

A

TARPS transmembrane AMPA receptor regulatory proteins

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21
Q

what does TARPS gamma 8 do?

A

modulates excitation activity in hypothalamus not LTP

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22
Q

what does phosphorylation of AMPAS do ?

A

increases conductance

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23
Q

what does camkinase 11 do?

A

phosphorylate AMPAs and increase the number of AMPAs at the surface of synapses

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24
Q

what is senescence ?

A

loss of cells power to divide and grow , acquires secretory phenotype in non dividing cells

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25
Q

what cells can senescence happen in ?

A

any - mainly rapidly dividing

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26
Q

what causes senescence ?

A

telomere alt - shortening, mitochondria dysfunction - caused by oxidative stress, epigenetic changes

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27
Q

what is the decision cells have to make when exposed to senescence stimulus?

A

growth arrest or replication

28
Q

what does cell arrest cause?

A

chronic low level inflammation which can lead to disease

29
Q

what can be used as markers to show senescence ?

A

cytokines

30
Q

what are the key features which change with age that could cause senescence ?

A

glucose metabolism changes , oxidative stress causes damage and decreased plasticity , protein processing changes and synaptic signalling of proteins changes

31
Q

what combines to create neurodegradation ?

A

protein aggregation and neural vulnerability

32
Q

how are parkinsons and schizophrenia linked?

A

park - low levels of dopamine , schiz- high levels

33
Q

whats the primary excitatory NT?

A

glutamate

34
Q

whats the primary inhibitor NT?

A

GABA

35
Q

two main dopamine pathways?

A

mesocortical dopamine pathway , nigoralstriatal

36
Q

is dopamine exc or inhib ?

A

can be both depending on which receptor it binds to

37
Q

whats bradykinesia ?

A

lack of activity

38
Q

what are the stages in park?

A

pre motor , diagnosis , adv motor and non motor , palliative

39
Q

what is the pathology of park?

A

cell loss and lewy body formation

40
Q

what can cause lewy body formation ?

A

oxidative stress, lysosomal function , mis folding of alpha synuclein genetic mutations

41
Q

whats idiopathic?

A

without a cause

42
Q

whats the role of synuclein ?

A

molecular chaperone - helps with folding of SNARES

43
Q

role of SNARES?

A

help release NTs

44
Q

how do lewy bodies form ?

A

alpha synuclein monomers for oligomers , these for, fibrils and aggregate into lewy bodies

45
Q

how can you treat dopamine deficiency

A

increase it , NT block and stimulate

46
Q

issues with just injecting dopamine ?

A

doesnt cross the blood brain barrier and doesnt effect none motor issues

47
Q

what is commoly used to treat low levels fo dopamine ?

A

l- dopa

48
Q

why do some using l-dopa appear to be drunk?

A

cause dopa occurs in peaks and troughs instead of being tonic

49
Q

what does camkinase do ?

A

increase LTP as it introduces Ampr subunits at the synapse

50
Q

how do glial cells control LTP ?

A

control levels of the coagonist for NMDAr as it needs glutamate and either serine or glycine

51
Q

WhatS BDNF ?

A

Brain derived neurotrophic factor

52
Q

what impact does stress have on neurons ?

A

decreases spines and synaptic connections - LTD

53
Q

what is ketamine ?

A

NMDAR antagonist - blocks NMDAR

54
Q

what could ket be used to treat depression ?

A

blocking of NMDAR on inhibitory neurone would increase excitation

55
Q

what is mTOR?

A

mammal target of rapamycin - regulates ageing and protein trans

56
Q

what is meta plasticity ?

A

plasticity of synpases - recent history of a synapses plastic activity influences its current level of reactivity

57
Q

why does levodopa cause dyskinesia ?

A

activates both d1/2 receptors and causes pulsatile dopamine - window of motor activation gets shorted with continued usage

58
Q

what factors influence the risk of dyskinesia ?

A

severity of park , age and therapy treatment ( dose and how long you’ve been on ldope )

59
Q

why do dopaminergic neurons get affected?

A

low oxidative stress responses

60
Q

whats UPR?

A

unfolded protein response

61
Q

what does UPR do?

A

causes inflammatory signals and ER stress

62
Q

what do alpha synuclein do ?

A

blocks degradation of unfolded proteins, protein transport out of the nucleus and disrupts protein folding

63
Q

what are the 3 Ns?

A

neurone protection, plasticity and repair

64
Q

what are retinoids ?

A

metabolites of vitamin a

65
Q

what happens to retinoids over time ?

A

they decrease along with their receptors

66
Q

what functions do retinoids have?

A

genomic and intracellular

67
Q

what are RARs?

A

retinoid acid receptors - which activate genes that prevent amyloid plaques forming

Ageing (3 decks)

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