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dumb brain > 8 - Neurodegenerative Diseases > Flashcards

8 - Neurodegenerative Diseases Flashcards

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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
Q

evidence against BAPs

A

B-amy found in those without Alzheimer’s, relationship with tau unclear, weak correlation between it and Alzheimer’s severity

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26
Q

evidence against BAP related to APOE4

A

it’s associated with other dementia types so not enough specificity

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27
Q

describe neurofibrillary tangles

A

made of tau, within cells, and affect nutrient movement and communication between/within nerve cells

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28
Q

what does tau do to microtubules

A

stabilises them by binding to 4 points

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29
Q

what happens when tau is hyperphosphorylated meaning it can’t bind to microtubules

A

tangles cause depolymerisation, impaired axonal transport, so neurotransmitters don’t get to terminal, nothing released, synapse dies, protein tangle left behind

30
Q

what is the keychain for the tau hypothesis

A

health neuron damages, tau in neuron released, immune response triggered, microglia activated, cytotoxins released, more damage

31
Q

evidence for tau hypothesis

A

tau levels correlate with AD severity

levels in CSF correlate with cognitive impairment

32
Q

evidence of tau related to oligomers

A

tau oligomers found in those who develop Alzheimer’s

33
Q

evidence for tay hypothesis related to treatment

A

those targeting tau are effective for cognitive impairment, symptoms treated using tau inhibitors in animals

34
Q

what is the first part of the amyloid cascade hypothesis

A

b-a clumps into oligomers then plaques which get into synapses causing dysfunction so neuroinflammation occurs

35
Q

neuroinflammation causes which cells tp be activated

A

microglial and astrocytic

36
Q

what is the second part of the amyloid cascade hypothesis

A

balance of Ca2+/K+ ions disrupted, phosphatase + kinase activity altered causing tangles, neuronal dysfunction occurs, neurons die

37
Q

PD: what happens when there is a mutation on chromosome 4

A

alpha-synuclein produced in pre-synaptic neurons affecting DA neuron synaptic transmission

38
Q

why is synaptic activity affected by chromosome 4 mutations

A

aggregations form leading to Lewy bodies forming and a toxic gain of function since they’re toxic to the cell

39
Q

PD: mutation for parkin prevents what

A

proteasomes receiving and destroying defective proteins so they build up and damage DA neurons instead

40
Q

what gene codes for Lewy bodies

A

Park1

41
Q

what risk factor of Alzheimer’s is also for Parkinson’s

A

repeated head trauma

42
Q

how do oxidative stress and free radicals cause PD

A

imbalance with reactive O2 species production and their clearance damages DNA, lipids, proteins - DA neurons more susceptible

43
Q

how are environmental toxins a risk for PD

A

can increase ox stress, mitochondrial dysfunction

44
Q

what can pesticides do to cause PD

A

inhibit mitochondria through mutations and reactive oxygen species so misfolded a-synuclein builds up

45
Q

how does MPTP contribute to PD development

A

striatal DA loss so less DA in subcortical regions, affecting the substantia nigra

46
Q

what is the primary pathway in PD where most loss occurs

A

nigrostriatal pathway, which is where PD starts

47
Q

what structure is affected in PD leading to less serotonin

A

serotonergic raphe nuclei

48
Q

in PD, where are Lewy bodies present abnormally

A

cytoplasm

49
Q

where are DA cells lost in PD

A

substantia nigra reticulata, which innervates basal ganglia, limbic forebrain, and cortex
subthalamic nucleus
globus pallidus

50
Q

what division of the basal ganglia is affected most by DA loss in PD

A

putamen as losing DA affects motor skills since it receives excitatory glutamate from motor areas

51
Q

describe receptors and role of the direct nigrostriatal pathway and indirect

A

D1 receptors, excites

D2 receptors, inhibits

52
Q

describe keychain of what dopamine usually does in the direct nigrostriatal pathway

A

cortex and SNc exc striatum, which inhibits GPi/SNr, which inhibit the thalamus, which exc the cortex

53
Q

describe the keychain of what dopamine usually does in the indirect pathway (motor loop)

A

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
Q

describe acetylcholinesterase inhibitors for treatment of Alzheimer’s

A

prevents ACh from being destroyed to improve motivation, memory, concentration but doesn’t affect neural degeneration

55
Q

describe NMDA receptor antagonists for Alzheimer’s treatment

A

blocks glutamate activity and slows ACh neuron degeneration, slows symptom progression, helps w delusions, agitation

56
Q

2 other Alzheimer’s treatments

A

psychosocial

antipsychotics

57
Q

how can L-DOPA treat PD

A

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
Q

why does L-DOPA need to be put in with dopamine decarboxylase inhibitor

A

so L-DOPA not converted to DA early but after it passes through b-b barrier as inhibitor won’t pass through

59
Q

2 negatives of using L-DOPA

A

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
Q

describe using dopamine agonists to mimic DA action

A

work at post-syn DA receptors to reduce motor complications but are weaker than DA

61
Q

how do MAOB and COMT inhibitors decrease dopamine breakdown

A

MAOB for early/late COMT for late both have symptom control and reduce motor complications but can’t control DA neuron degeneration

62
Q

what’s one method to reduce motor complications only

A

decrease reuptake and increase release

63
Q

why would the globus pallidus be destroyed to treat parkinson’s

A

less dopamine means more GP activity which inhibits the motor cortex through the subthalamic nucleus

64
Q

how does deep brain stimulation work

A

STN/GP have rhythm imposed so they synchronise and reduce dyskinesias

65
Q

how can transplanting foetal dopaminergic neurons from the substantia nigra help to treat parkinson’s

A

transplant into basal ganglia so differentiate into neurons, astrocytes, and oligodendrocytes to improve motor and bhvrl symptoms but Lewy bodies still spread

66
Q

how can induced pluripotent stem cells be used to treat Parkinson’s

A

SCNT to differentiate into neurons, astrocytes, oligodendrocytes, and reinnervate host brain to improve motor function

67
Q

stem cells are used to do what to treat Parkinson’s

A

development in dopamine producing nerve cells so dopamine can transmit nerve signals

68
Q

how can gene therapy be used to treat Parkinson’s

A

prevents cell death and promotes regeneration by increasing L-DOPA/DA levels

69
Q

what is the process in gene therapy to lower GP activity

A

insert GAD gene into virus, mix with extracted cells from patient and then reinsert

70
Q

why is GAD used in gene therapy

A

it produces GABA which is inhibitory so it replaces excitatory glutamate neurons in the STN to decrease GP activity

71
Q

issues with gene therapy

A

safety of viruses and gene expression

72
Q

how can tremors and rigidity be treated

A

stereotactic neurosurgery to create lesions in the brain

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