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PSY2013- Biological Psychology with Research Methods 2 > 7- Neurodegenerative Diseases > Flashcards

7- Neurodegenerative Diseases Flashcards

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1
Q

How is dementia defined?

A

A loss of cognitive functioning interfering with someone’s daily life and activities

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2
Q

What is the global prevalence of dementia?

A

About 46 million people in 2015

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3
Q

What is the expected trend of dementia?

A

To increase as the population ages

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4
Q

5 types of dementia

A
  1. Alzheimer’s Disease- most common
  2. Vascular dementia
  3. Posterior cortical atrophy
  4. Lewy body dementia
  5. Frontotemporal dementia
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5
Q

How many cases of dementia are Alzheimer’s Disease?

A

50-70%

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6
Q

What is the Alzheimer’s prevalence at 55 years?

A

0.5%

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7
Q

How does the risk of Alzheimer’s change as one ages?

A

Doubles every 5 years

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8
Q

How many new cases of Alzheimer’s each year?

A

About 7.7 million

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9
Q

How often is someone diagnosed globally with Alzheimer’s?

A

Every 4 seconds

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10
Q

What type of Alzheimer’s show a clear inheritance pattern?

A

Early-onset familial Alzheimer’s

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11
Q

How many studies have identified specific genes responsible for Alzheimer’s?

A

A minority

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12
Q

What is Alzheimer’s preceded by?

A

Mild Cognitive Impairment phase

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13
Q

Where are initial Alzheimer’s symptoms?

A

In the memory domain, but progress to other domains

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14
Q

What disturbances are observed in later stages of Alzheimer’s?

A

Mood and behavioural disturbances

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15
Q

How long can mild to severe Alzheimer’s progression take?

A

Up to 10 years

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16
Q

7 symptoms of mild Alzheimer’s

A
  • Forgetfulness
  • Word finding difficulty
  • Apathy
  • Poor attention
  • Complex task difficulty
  • Depression
  • Work trouble
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17
Q

8 symptoms of moderate Alzheimer’s

A
  • Disorientation
  • Increased memory loss
  • Confusion
  • Insomnia
  • Wandering
  • Speech difficulty
  • Restlessness
  • Difficulty with everyday activities
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18
Q

7 symptoms in severe Alzheimer’s

A
  • Agnosia
  • Apraxia
  • Aggression
  • Agitation
  • Incontinence
  • Poor basic everyday activities
  • Gait disturbance
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19
Q

What is the main drug therapy for Alzheimer’s and what is the aim?

A

Cholinesterase inhibitors, aim to increase acetylcholine in the brain

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20
Q

When were cholinesterase inhibitors discovered?

A

25 years ago

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21
Q

What functions is acetylcholine’s role established in?

A

Learning and memory

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22
Q

What happens to acetylcholine at the synapse?

A

It is broken down by acetylcholinesterase

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23
Q

How do acetylcholinesterase inhibitors (AChEIs) increase acetylcholine?

A

By blocking the enzyme

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24
Q

What does the cholinergic hypothesis suggest is the cause of Alzheimer’s?

A

Loss of cholinergic neurons

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25
Q

What did post-mortem studies in the mid-1970s find?

A

Reduced levels of the enzyme responsible for acetylcholine synthesis in the cortex

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26
Q

How do acetylcholinesterase inhibitors help compensate for cholinergic neurons?

A

By boosting Ach

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27
Q

How many cases do AChEIs offer symptomatic improvement in?

A

About 50%

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28
Q

How long are cognition improvements sustained for after treatment with AChEIs?

A

For about 2 years

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29
Q

2 limitations of AChEIs treatment

A
  1. Not ‘disease modifying’
  2. Modest and temporary symptom improvement only- doesn’t slow course of the disease
30
Q

Why is the cholinergic hypothesis no longer favoured for treatment?

A

Treatment has limited effects

31
Q

What might cholinergic system failure also be due to?

A

Accumulation of other pathology

32
Q

Is Ach the only neurotransmitter affected by Alzheimer’s?

A

No, nor is it the only neurodegenerative disorder that shows cholinergic dyfunction

33
Q

What 2 things occur in the brains of Alzheimer’s patients?

A

Amyloid-beta plaques and neurofibrillary tangles

34
Q

What is brain shrinkage like in Alzheimer’s brain?

A

It begins in hippocampal formation and spreads, is consistent with symptoms

35
Q

What is amyloid beta?

A

A fragment of larger protein called APP found in healthy neurons

36
Q

What leads to higher levels of amyloid beta in Alzheimer’s?

A

Abnormal cleavage of APP

37
Q

How are plaques created?

A

Amyloid beta 42 aggregates into ‘clumps’

38
Q

What do plaques trigger?

A

An inflammatory response

39
Q

What does the inflammatory response triggered by plaques lead to?

A

Synaptic dysfunction and neuronal death

40
Q

How can the progression of amyloid plaques be detected in Alzheimer’s?

A

PET brain imaging can detect plaques

41
Q

How do plaques follow a characteristic pattern?

A

As Alzheimer’s progresses

42
Q

Where do amyloid plaques begin?

A

In hippocampal regions

43
Q

How do amyloid plaques spread in Alzheimer’s?

A

Spreads to temporal lobe to frontal to eventually affecting the entire cortex

44
Q

How is tau protein different to amyloid?

A

Seems to build up after amyloid

45
Q

What is the amyloid cascade hypothesis?

A

Believes that amyloid beta is the initiating event in Alzheimer’s, which then triggers symptoms and other pathology

46
Q

When are amyloid plaques detectable in Alzheimer’s?

A

Very early in the disease process

47
Q

What has been the dominant theory of AD pathogenesis since the 90s?

A

Amyloid cascade hypothesis

48
Q

What type of AD implicates genes involved in production of the precursor of beta-amyloid protein?

A

Familial AD

49
Q

What is the problem with the amyloid cascade hypothesis?

A

Amyloid load doesn’t link well with AD symptom severity

50
Q

What evidence shows that amyloid may not be predictive of AD?

A

30% of cognitively normal controls show elevated amyloid

51
Q

What does high amyloid increase risk of?

A

Later cognitive decline

52
Q

What does high amyloid predict?

A

Conversion from Mild Cognitive Impairment to AD

53
Q

What are the 2 strategies of anti-amyloid drugs?

A
  1. Block/inhibit overproduction or aggregation of AB- inhibit enzymes which break down APP into AB
  2. Clearance of AB from brain
54
Q

What does blocking overproduction of AB increase risk of?

A

Skin cancer and infections- significant negative effects on function and cognition

55
Q

How do anti-amyloid drugs promote AB clearance from the brain?

A

Antibodies that bind to the AB peptide and speed up clearance

56
Q

What do anti-amyloid drugs show evidence for but what not for?

A

Evidence for enhanced clearance, no effect on symptom progression

57
Q

3 disadvantages of anti-amyloid drugs

A

Limited effects on symptoms
High costs
Risk of side-effects

58
Q

What type of protein is tau protein?

A

An intracellular protein

59
Q

What does tau protein do?

A

Stabilises microtubules that transport nutrients and molecules from the cell body to the axon and dendrites

60
Q

How are neurofibrillary tangles formed?

A

By abnormal chemical changes that cause tau to become ‘hyperphosphorylated’ and clump together

61
Q

What is the effect of neurofibrillary tangles?

A

Impair microtubule function

62
Q

What is the second most common cause of dementia?

A

Vascular dementia

63
Q

What happens in vascular dementia?

A

Loss of cognitive functioning due to a series of small ‘silent’ strokes

64
Q

What is the main symptom of vascular dementia?

A

Progressive cognitive impairment after each stroke

65
Q

5 risk factors of vascular dementia

A

Age
Hypertension
Smoking
High cholesterol
Diabetes

66
Q

Why is early detection of vascular dementia essential?

A

Treatment involves reducing the risk factors

67
Q

Why can diagnosis of vascular dementia be difficult?

A

Since features overlap with other dementias

68
Q

What is PCA?

A

An atypical variant of Alzheimer’s

69
Q

How is PCA characterised in the brain?

A

Focal, affecting posterior parietal cortex

70
Q

5 symptoms of PCA

A
  • Blurred vision, light sensitivity
  • Progressive inability to recognise faces and objects
  • Problems with spatial skills such as dressing and driving
  • Impaired reading and writing
  • Memory, spoken language and reasoning better preserved until later stages

PSY2013- Biological Psychology with Research Methods 2 (37 decks)

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