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8 - Neurodegenerative Diseases Flashcards

1
Q

what is Alzheimer’s and who’s most likely to suffer

A

most common dementia type

White and women

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2
Q

symptoms of Alzheimer’s

A

memory loss/change
using inappropriate words
personality changes
problems with understanding and verbal tasks

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3
Q

risk factors of Alzheimer’s

A

alcohol
smoking
genetics

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4
Q

why is social isolation a risk factor of Alzheimer’s

A

no one to practice speech and understanding and not taking in social activities means cognitive functioning can’t be maintained

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5
Q

why is diet and physical activity a risk factor of Alzheimer’s

A

higher BMI and less physical activity correlate with lower cognitive health

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6
Q

why is poor education a risk factor of Alzheimer’s

A

not keeping brain active and is a strong predictor although could just be socioeconomic status

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7
Q

why does head trauma quicken the onset of Alzheimer’s

A

widespread plaques and having APOE4 gene reduces recovery

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8
Q

what is PD and its prevalence and incidence rates

A

second most common dementia with 1 in 500 having it and incidence being 1/12 of prevalence rate

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9
Q

what are some motor symptoms of PD

A

rigidity, forward tilt of trunk, shuffling gait, brady/hypokinesia

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10
Q

what are some non-motor symptoms of PD

A

impaired memory, fluctuating attention, impaired perception, mood problems

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11
Q

describe the gross pathology of Alzheimer’s

A

frontal/temp lobes lose volume

enlarged sulci

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12
Q

in Alzheimer’s, what does a loss in hippocampus mean

A

memory is affected and this correlates with rate of cognitive loss

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13
Q

in Alzheimer’s, what does reduces brain activity during facial recognition tests mean

A

there is no activity so people and places are confused

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14
Q

in Alzheimer’s, what does neuronal loss mean

A

decline in ChAT/cholinergic neurons impacting memory and cognition as less ACh

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15
Q

where are beta amyloid plaques and what do they do

A

in between cells and in synapses, interfere with cell communication

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16
Q

what are BAPs made of

A

amyloid precursor protein which is on chromosome 21 and is responsible for synapse formation and neuronal plasticity

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17
Q

what is APP split into

A

alpha, beta, gamma secretases

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18
Q

in the non-amyloid pathway, what processes happen

A

alpha secretase splits APP and then gamma secretase splits the strand in the membrane into 2

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19
Q

what happens in the amyloid pathway

A

beta-secretase cuts instead and then gamma-sec splits membrane strand into 2, including a B-amyloid strand

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20
Q

why does too much BAP lead to Alzheimer’s

A

they stimulate receptors responsible for apoptosis

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21
Q

why do more BAPs form

A

Presenilin 1/2 mutations responsible for gamma-sec

APOE4 mutation means BAPs not cleared up

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22
Q

BAP evidence related to C21

A

those with triple C21 develop it and have plaques

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23
Q

BAP evidence related to oligomers

A

they decrease synaptic density and cause long-term synaptic depression, impairing memory

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24
Q

evidence: what happens when B-amyloid is cultures in neurons

A

tau is produced

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25
evidence against BAPs
B-amy found in those without Alzheimer's, relationship with tau unclear, weak correlation between it and Alzheimer's severity
26
evidence against BAP related to APOE4
it's associated with other dementia types so not enough specificity
27
describe neurofibrillary tangles
made of tau, within cells, and affect nutrient movement and communication between/within nerve cells
28
what does tau do to microtubules
stabilises them by binding to 4 points
29
what happens when tau is hyperphosphorylated meaning it can't bind to microtubules
tangles cause depolymerisation, impaired axonal transport, so neurotransmitters don't get to terminal, nothing released, synapse dies, protein tangle left behind
30
what is the keychain for the tau hypothesis
health neuron damages, tau in neuron released, immune response triggered, microglia activated, cytotoxins released, more damage
31
evidence for tau hypothesis
tau levels correlate with AD severity | levels in CSF correlate with cognitive impairment
32
evidence of tau related to oligomers
tau oligomers found in those who develop Alzheimer's
33
evidence for tay hypothesis related to treatment
those targeting tau are effective for cognitive impairment, symptoms treated using tau inhibitors in animals
34
what is the first part of the amyloid cascade hypothesis
b-a clumps into oligomers then plaques which get into synapses causing dysfunction so neuroinflammation occurs
35
neuroinflammation causes which cells tp be activated
microglial and astrocytic
36
what is the second part of the amyloid cascade hypothesis
balance of Ca2+/K+ ions disrupted, phosphatase + kinase activity altered causing tangles, neuronal dysfunction occurs, neurons die
37
PD: what happens when there is a mutation on chromosome 4
alpha-synuclein produced in pre-synaptic neurons affecting DA neuron synaptic transmission
38
why is synaptic activity affected by chromosome 4 mutations
aggregations form leading to Lewy bodies forming and a toxic gain of function since they're toxic to the cell
39
PD: mutation for parkin prevents what
proteasomes receiving and destroying defective proteins so they build up and damage DA neurons instead
40
what gene codes for Lewy bodies
Park1
41
what risk factor of Alzheimer's is also for Parkinson's
repeated head trauma
42
how do oxidative stress and free radicals cause PD
imbalance with reactive O2 species production and their clearance damages DNA, lipids, proteins - DA neurons more susceptible
43
how are environmental toxins a risk for PD
can increase ox stress, mitochondrial dysfunction
44
what can pesticides do to cause PD
inhibit mitochondria through mutations and reactive oxygen species so misfolded a-synuclein builds up
45
how does MPTP contribute to PD development
striatal DA loss so less DA in subcortical regions, affecting the substantia nigra
46
what is the primary pathway in PD where most loss occurs
nigrostriatal pathway, which is where PD starts
47
what structure is affected in PD leading to less serotonin
serotonergic raphe nuclei
48
in PD, where are Lewy bodies present abnormally
cytoplasm
49
where are DA cells lost in PD
substantia nigra reticulata, which innervates basal ganglia, limbic forebrain, and cortex subthalamic nucleus globus pallidus
50
what division of the basal ganglia is affected most by DA loss in PD
putamen as losing DA affects motor skills since it receives excitatory glutamate from motor areas
51
describe receptors and role of the direct nigrostriatal pathway and indirect
D1 receptors, excites | D2 receptors, inhibits
52
describe keychain of what dopamine usually does in the direct nigrostriatal pathway
cortex and SNc exc striatum, which inhibits GPi/SNr, which inhibit the thalamus, which exc the cortex
53
describe the keychain of what dopamine usually does in the indirect pathway (motor loop)
cortex exc striatum, which inhibits the GPe, which inhibits the STN, which exc the GPi/SNr, which inhibits the thalamus, which exc the cortex
54
describe acetylcholinesterase inhibitors for treatment of Alzheimer's
prevents ACh from being destroyed to improve motivation, memory, concentration but doesn't affect neural degeneration
55
describe NMDA receptor antagonists for Alzheimer's treatment
blocks glutamate activity and slows ACh neuron degeneration, slows symptom progression, helps w delusions, agitation
56
2 other Alzheimer's treatments
psychosocial | antipsychotics
57
how can L-DOPA treat PD
affects DA neurons in the mesolimbic and mesocortical systems to control symptoms e.g. tremors, which can be done as more D2 receptors in striatum
58
why does L-DOPA need to be put in with dopamine decarboxylase inhibitor
so L-DOPA not converted to DA early but after it passes through b-b barrier as inhibitor won't pass through
59
2 negatives of using L-DOPA
tyrosine hydroxylate is rate limiting so adding more L-DOPA won't make a difference wears off as more DA terminals lost in the long-term
60
describe using dopamine agonists to mimic DA action
work at post-syn DA receptors to reduce motor complications but are weaker than DA
61
how do MAOB and COMT inhibitors decrease dopamine breakdown
MAOB for early/late COMT for late both have symptom control and reduce motor complications but can't control DA neuron degeneration
62
what's one method to reduce motor complications only
decrease reuptake and increase release
63
why would the globus pallidus be destroyed to treat parkinson's
less dopamine means more GP activity which inhibits the motor cortex through the subthalamic nucleus
64
how does deep brain stimulation work
STN/GP have rhythm imposed so they synchronise and reduce dyskinesias
65
how can transplanting foetal dopaminergic neurons from the substantia nigra help to treat parkinson's
transplant into basal ganglia so differentiate into neurons, astrocytes, and oligodendrocytes to improve motor and bhvrl symptoms but Lewy bodies still spread
66
how can induced pluripotent stem cells be used to treat Parkinson's
SCNT to differentiate into neurons, astrocytes, oligodendrocytes, and reinnervate host brain to improve motor function
67
stem cells are used to do what to treat Parkinson's
development in dopamine producing nerve cells so dopamine can transmit nerve signals
68
how can gene therapy be used to treat Parkinson's
prevents cell death and promotes regeneration by increasing L-DOPA/DA levels
69
what is the process in gene therapy to lower GP activity
insert GAD gene into virus, mix with extracted cells from patient and then reinsert
70
why is GAD used in gene therapy
it produces GABA which is inhibitory so it replaces excitatory glutamate neurons in the STN to decrease GP activity
71
issues with gene therapy
safety of viruses and gene expression
72
how can tremors and rigidity be treated
stereotactic neurosurgery to create lesions in the brain

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