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Clinical Ageing > Dementia > Flashcards

Dementia Flashcards

1
Q

How many dementia cases are Alzheimer’s?

A

60%

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2
Q

Where does Alzheimer’s and other dementias rank globally for causes of death?

A

Roughly third across the tables

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3
Q

What can cause reversible cognitive decline?

A

Thyroid disorder - having low folate/ Low B12

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4
Q

Is neurodegeneration reversible?

A

No - and it could be vascular related

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5
Q

What test is used to diagnosis Alzheimer’s?

A

MOCA test = Montreal Cognitive Assessment

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6
Q

Describe the MOCA test

A
  1. 5 random words
  2. 3 images
  3. easy question (name as many words beginning with the letter F in one minute)
  4. recall test a bit later on
    marked for each section and answers collated
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7
Q

What is the issue with dementias having similar clinical presentation

A

easy to get a differential diagnosis - getting the wrong treatment for the wrong diagnosis

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8
Q

what do neurodegenerative dementias share?

A

basic processes

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9
Q

How do neurodegen dementias differ?

A

Pathologically different and different areas are affected

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10
Q

what is the typical aetiology of neurodegen dementias?

A

protein aggregates - misfolded/ deposition

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11
Q

Of what percentage of all Alzheimer’s cases are from young people?

A

31

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12
Q

When was Alzheimer’s First described?

A

1906 - rare disorder of a young onset, when previously seen in elderly

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13
Q

What did Tomlinson describe in 1960s?

A

Senile dementia - subgroup later to be called Alzheimer’s - progressive cog decline, psychiatric features, post-mortem confirmed

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14
Q

How many questions are there within the Hachinski Ischaemia Score?

A

12

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15
Q

What does Hachinski Score do?

A

differentiate between different dementias

  • scoring 4 - primary dementia
  • scoring 4-7 - indeterminate
  • scoring 7+ - vascular dementia

used to detect vascular dementia

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16
Q

what are the 8 questions within Hachinski Score that score one point each?

A
  1. nocturnal confusion
  2. stepwise deterioration
  3. emotional incontinence
  4. depression
  5. history of hypertension
  6. atherosclerosis
  7. somatic complaints
  8. change in personality
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17
Q

what are somatic complaints?

A

the fixation on a physical problem eg SoB, pain

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18
Q

What 4 questions score 2 points each on the HIS diagnostic quiz?

A
  1. fluctuating score
  2. focal neuro symptoms
  3. history of strokes
  4. focal neuro signs
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19
Q

what are the three things within the cholinergic hypothesis?

A
  1. reduced choline acetyltransferase
  2. altered pattern of acetylcholinesterase
  3. loss of cholinergic neurones in basal forebrain
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20
Q

What is the implication of reduced choline acetyltransferase?

A

within cholinergic hypothesis
this enzyme then produces less ACh, therefore it has a smaller ability to dilate blood vessels, it can also slow heart rate - will not be able to as fast with a smaller conc

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21
Q

what is the implication of altered pattern of acetylcholinesterase?

A

within the cholinergic hypothesis

this enzyme hydrolyses ACh - will do this function at wrong time/ insufficiently

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22
Q

what are the implications of loss of cholinergic neurones in the basal forebrain?

A

Neurones here are responsible for learning, memory and attention
- less efficient

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23
Q

Name 2 ACh inhib that is used within cholinergic monotherapy?

A
  • Donepezil known as the brand name of Aricept

- Galanthamine known as Reminyl and Nivalin

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24
Q

Name a cholinergic monotherapy that is an ACh inhib and BCH inhib

A

Rivastigmine known as Excelon

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25
Q

what is BCHe?

A

inhibitor that blocks neuromuscular agents

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26
Q

what is the side effects of cholinergic monotherapy

A

turn on all the taps

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27
Q

Describe the neuropathy of Alzheimer’s Disease

A
  1. alpha beta deposits - aggregation of protein, which is the amyloid precursor protein
  2. neurofibrillary tangles
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28
Q

what is the size of AB aggregation protein?

A

40-42 amino acids

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29
Q

what compound can all imaging of AB?

A

Pittsburgh compound B

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30
Q

how does alpha beta mediated therapy work?

A

mediated by microglia - breaks plaques into single strips

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31
Q

what is the name of the drug that acts as a alpha -beta mediated therapy

A

aducanumab - reduces plaques

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32
Q

what are the tau levels within Alzheimer’s?

A

high

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33
Q

what are the alpha beta levels within Alzheimer’s?

A

low

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34
Q

how does tau detach from a microtubule?

A

kinase mediated phosphorylation

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35
Q

after phosphorylation and tau detaches from microtubule what happens?

A

aggregation is promoted

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36
Q

what does PET scans for within the diagnosis of AD?

A

screens for tau - due to the neuroanatomical variability

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37
Q

what has a distinct uptake that causes tau pathology within AD?

A

18F- AV1451

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38
Q

what can be shown within CSF tests?

A

AB1-42, T- tau, P tau181

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39
Q

what are the advantages of using CSF?

A

has distinct markers, earlier diagnosis than blood work

40
Q

what does blood work show within AD diagnosis?

A

p-tau217

41
Q

what are the advantages of blood work within AD diagnosis?

A

easier to retrieve, less uncomfortable

42
Q

why is PTau 181 so useful from CSF?

A

it is a neuronal fibrillary tangle protein, which is specific to AD - shows cognitive decline

43
Q

what is the amyloid hypothesis?

A

the alpha beta related toxicity causing synaptic dysfunction

43
Q

what is the amyloid hypothesis?

A

the alpha beta related toxicity causing synaptic dysfunction

44
Q

what does aducanumab B11B037 do?

A

it is a human monoclonal antibody which selects aB- aggregates

45
Q

how long does it take for aB aggregates to accumulate to reach the level of mild AD?

A

about 20 years

46
Q

what was the name of the aducamunab drug study?

A

Sevigny, 2016

47
Q

what was the Sevigny, 2016 study?

A

a randomised multicentre double blinded study with follow ups - using aducanumab to select aB

48
Q

what were the documented side effects of using aducanumab as drug to select aB plaques?

A

headaches, UTI, respiratory infections

49
Q

what was the AD study assessing CSF biomarkers?

A

Neimantsverdriet, 2017

50
Q

how does the 2017 study describe a lumbar puncture

A

more tolerable than expected, low complication rate, high diagnostic yield
more direct to neuropathy, cheaper than a PET scan

51
Q

what diagnostic test can be used to assess protein levels within the blood?

A

SIMOA

52
Q

what is SIMOA?

A

ultra-sensitive immunoassay that detects proteins at very low levels

53
Q

what protein can SIMOA detect?

A

ptau181 - specific to AD

54
Q

what is a hallmark of AD?

A

the accumulation of amyloid beta plaques in the brain

55
Q

what is the main Amyloid beta protein?

A

AB1-42

56
Q

what is elevated homocysteine associated to?

A

AD and strokes

57
Q

what are hallmarks of B12 deficiencies which can cause reversible cognitive decline?

A

elevated homocysteine and elevated methylmalonic acid

58
Q

what can the elevated homocysteine and low B12 do to the brain?

A

silent brain injury through oxidative stress, ca2+ influx, apoptosis

59
Q

what can interfere with vit B12 release from food sources

A

proton pump inhibitors eg lansoprazole

H2 receptor blocking agent (histamines)

60
Q

what can prolonged B12 deficiency lead to in elderly?

A

can lead to irreversible cognitive impairment if it continues to deteriorate

61
Q

how common is vascular dementia?

A

the second most common dementia after AD

62
Q

what is vascular dementia?

A

decreased blood flow to the brain tissue - can be a partial block that can become completely blocked by a blood clot

63
Q

what is the difference between a stroke and vascular dementia?

A

vascular dementia is a narrowing which decreases blood flow to the brain but a stroke is a complete block that occurs suddenly

64
Q

what is MoCA scored to?

A

0-30

65
Q

what is a normal MOCA score?

A

26/30

66
Q

what score would indicate mild cognitive impairment within a MOCA test?

A

on average about 22

67
Q

what is the average score on a MOCA test in AD patients?

A

16.2/30

68
Q

why is MOCA used more than MMSE test?

A

it is more sensitive

can identify cognitive impairments within patients with Parkinson’s

69
Q

what is MMSE?

A

mini mental state examination

70
Q

what is MMSE scored to?

A

0-30

71
Q

what is a normal score in MMSE?

A

24 or higher out of 30

72
Q

in MMSE would scores would suggest mild cog impairment?

A

18-23

73
Q

In MMSE what score would indicate severe cognitive impairment?

A

0-17

74
Q

what does MMSE test?

A

orientation, attention, memory, language, visual spatial skills

75
Q

in AD what would a MRI show?

A

diffuse atrophy within temporal and frontal lobes

76
Q

what is the role of tau in normal functioning brains?

A

stabilises internal microtubules

77
Q

what do neurofibrillary tangles contain?

A

tau

78
Q

how does taus function change?

A

chemical alterations by phosphorylation causing tau to detach from microtubule and they can not bind back

79
Q

what occurs when the chemicals are changed within tau?

A

it can cause disorganisation, smaller fragments of tau circulates among neurones and this interferes with cellular function

80
Q

what has research suggested tau spreads and migrates within the brain?

A

by oligomer seeds that travel across the synapse and when not bound to microtubule it causes aggregation

81
Q

in AD, in both older and early onset where is 18f-AV1451 have high uptake?

A

grey matter in comparison to white matter

82
Q

what compromises of grey matter?

A

neuronal cell bodies, dendrites, unmyelinated axons, glial cells, synapses, capillaries

83
Q

what makes up white matter?

A

myelinated axons - gives it the colour

84
Q

in AD, what forms paired helical conformations?

A

18F-AV1451 with tau

85
Q

as well as in AD, what is 18F-AV1451 also seen in?

A

corticobasal degeneration (CSB) and progressive supranuclear palsy - atypical parkinsons

86
Q

what are are the 2 main pathological features of AD?

A

beta -amyloid plaques between neurones and neurofibrillary tangles containing tau between neurones that impact neuronal communication

87
Q

what part of the brain does Alzheimer’s originate from?

A

hippocampus and entorhinal cortex - hence memories are impacted

88
Q

what are the RF for AD?

A

age, family history, head injuries, CVD conditions

89
Q

what is RT-QuIC?

A

real time quaking induced assay

90
Q

what is the function of RT-QuIC?

A

in vitro amplification of abnormal prion protein (PrPSc) - quantifies prion seeding activity, only requires minute amounts

91
Q

what sample is best to use in RT-QuIC?

A

CSF - less other things in it

92
Q

what is Creutzfold-Jakob disease?

A

incurable neurodegenerative disease characterised progressive spongiform changes and the accumulation of abnormal prion protein in CNS

93
Q

what are the causes of CJD?

A

85% are sporadic, the remaining are genetic or infectious linked

94
Q

why is RT-QuIC better than sonification?

A

easier method and more consistent

Clinical Ageing (10 decks)

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