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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
what cells can senescence happen in ?
any - mainly rapidly dividing
26
what causes senescence ?
telomere alt - shortening, mitochondria dysfunction - caused by oxidative stress, epigenetic changes
27
what is the decision cells have to make when exposed to senescence stimulus?
growth arrest or replication
28
what does cell arrest cause?
chronic low level inflammation which can lead to disease
29
what can be used as markers to show senescence ?
cytokines
30
what are the key features which change with age that could cause senescence ?
glucose metabolism changes , oxidative stress causes damage and decreased plasticity , protein processing changes and synaptic signalling of proteins changes
31
what combines to create neurodegradation ?
protein aggregation and neural vulnerability
32
how are parkinsons and schizophrenia linked?
park - low levels of dopamine , schiz- high levels
33
whats the primary excitatory NT?
glutamate
34
whats the primary inhibitor NT?
GABA
35
two main dopamine pathways?
mesocortical dopamine pathway , nigoralstriatal
36
is dopamine exc or inhib ?
can be both depending on which receptor it binds to
37
whats bradykinesia ?
lack of activity
38
what are the stages in park?
pre motor , diagnosis , adv motor and non motor , palliative
39
what is the pathology of park?
cell loss and lewy body formation
40
what can cause lewy body formation ?
oxidative stress, lysosomal function , mis folding of alpha synuclein genetic mutations
41
whats idiopathic?
without a cause
42
whats the role of synuclein ?
molecular chaperone - helps with folding of SNARES
43
role of SNARES?
help release NTs
44
how do lewy bodies form ?
alpha synuclein monomers for oligomers , these for, fibrils and aggregate into lewy bodies
45
how can you treat dopamine deficiency
increase it , NT block and stimulate
46
issues with just injecting dopamine ?
doesnt cross the blood brain barrier and doesnt effect none motor issues
47
what is commoly used to treat low levels fo dopamine ?
l- dopa
48
why do some using l-dopa appear to be drunk?
cause dopa occurs in peaks and troughs instead of being tonic
49
what does camkinase do ?
increase LTP as it introduces Ampr subunits at the synapse
50
how do glial cells control LTP ?
control levels of the coagonist for NMDAr as it needs glutamate and either serine or glycine
51
WhatS BDNF ?
Brain derived neurotrophic factor
52
what impact does stress have on neurons ?
decreases spines and synaptic connections - LTD
53
what is ketamine ?
NMDAR antagonist - blocks NMDAR
54
what could ket be used to treat depression ?
blocking of NMDAR on inhibitory neurone would increase excitation
55
what is mTOR?
mammal target of rapamycin - regulates ageing and protein trans
56
what is meta plasticity ?
plasticity of synpases - recent history of a synapses plastic activity influences its current level of reactivity
57
why does levodopa cause dyskinesia ?
activates both d1/2 receptors and causes pulsatile dopamine - window of motor activation gets shorted with continued usage
58
what factors influence the risk of dyskinesia ?
severity of park , age and therapy treatment ( dose and how long you've been on ldope )
59
why do dopaminergic neurons get affected?
low oxidative stress responses
60
whats UPR?
unfolded protein response
61
what does UPR do?
causes inflammatory signals and ER stress
62
what do alpha synuclein do ?
blocks degradation of unfolded proteins, protein transport out of the nucleus and disrupts protein folding
63
what are the 3 Ns?
neurone protection, plasticity and repair
64
what are retinoids ?
metabolites of vitamin a
65
what happens to retinoids over time ?
they decrease along with their receptors
66
what functions do retinoids have?
genomic and intracellular
67
what are RARs?
retinoid acid receptors - which activate genes that prevent amyloid plaques forming

Ageing (3 decks)

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