26.10 - Cognitive Disorders of Old Age Flashcards

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1
Q

Compare how cognition changes in normal ageing and dementia.

A
  • Cognition is on a specturm, becoming more widely distributed with age
  • Between normality and dementia, there is a state of mild cognitive impairment, which can be considered as the prodrome of dementia
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2
Q

Do all types of cognition decline with age?

A
  • Most types of cognition decline with age, including:
    • Working memory
    • Processing speed
    • Long-term memory
    • Reasoning
  • The only exception is semantic memory and crystallised intelligence.
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3
Q

Is skill learning affected by ageing?

A

It is preserved, but it might just take longer.

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4
Q

What represents ageing more accurately: cross-sectional or longitudinal studies?

A
  • Cross-sectional studies tend to over-estimate the effects of ageing because younger participants are likely to be more familiar with technology used (e.g. tablets)
  • Longitudinal studies tend to under-estimate the effects of ageing because the participants get used to the method of assessing them and therefore do not appear to decline as much
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5
Q

Are all parts of the brain atrophied in ageing?

A

No, different parts atrophy to different extents. The hippocampus in particular tends to atrophy significantly.

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6
Q

What is the Oxford cognitive screen?

[EXTRA]

A

A chart developed to help record the functional deficiencies that patients with various brain lesions have.

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7
Q

What are 3 commonly reported phenomena seen in ageing?

A
  1. Overactivity of relevant brain areas when performing a task (Smith, 2001)
  2. Reductions in hemispheric asymmetry in functions such as language (Cabeza, 2002)
  3. Shift from posterior to anterior brain activity (Davis, 2008)
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8
Q

Describe what defines successful ageing. Give some experimental evidence.

A

(Cabeza, 2002):

  • Studied participants performing a language task
  • Young participants showed high asymmetry between the hemispheres
  • Low-functioning older participants maintained this symmetry, but had low brain activity
  • High-functioning older participants did not show such great asymmetry but showed much higher activity in both hemispheres

This can be explained by several theories:

  • Compensation -> There is additional recruitment of neural activity to maintain performance
  • De-differentiation -> There is loss of regional specificity
  • Scaffolding -> There is a dynamic ongoing process of plasticity
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9
Q

Describe the prevalence of dementia.

A
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10
Q

What are some causes of dementia mentioned in the spec and how common are they?

[IMPORTANT]

A
  • Alzheimer’s disease -> 60-80%
  • Fronto-temporal dementia -> 5-20%
  • Vascular dementia -> 5-15%
  • Lewy body disease -> 2-8%
  • Creutzfeldt–Jakob disease (prion disease) -> Rare
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11
Q

For dementia caused by Alzheimer’s disease, describe the prevalence, pathology and the primary site/features.

A
  • Prevalence: 60-80%
  • Pathology: Amyloid plaques and tau tangles
  • Site/Features: Medial temporal lobe and parietal lobe -> Then progresses to frontal areas
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12
Q

For fronto-temporal dementia, describe the prevalence, pathology and the primary site/features.

A
  • Prevalence: 5-20%
  • Pathology: Several subtypes involving the aggregation of proteins such as tau, TDP43 or FUS
  • Site/Features: Frontal lobe (behavioural symptoms) or temporal lobe (semantic/aphasia symptoms)
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13
Q

For vascular dementia, describe the prevalence, pathology and the primary site/features.

A
  • Prevalence: 5-15%
  • Pathology: Vascular pathology (e.g stroke)
  • Site/Features: Can be anywhere, Sudden changes, Step-wise progression
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14
Q

For dementia with Lewy bodies, describe the prevalence, pathology and the primary site/features.

A
  • Prevalence: 2-8%
  • Pathology: Lewy bodies (also seen in Parkinson’s disease)
  • Site/Features: Motor symptoms, Sleep disturbance (similar to in Parkinson’s disease), Visual hallucinations, Fluctuating deficits
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15
Q

For dementia due to Creutzfeldt–Jakob disease, describe the prevalence, pathology and the primary site/features.

A
  • Prevalence: Rare
  • Pathology: Prion protein deposition
  • Site/Features: ADD
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16
Q

What are the different causes of Alzheimer’s disease?

A
  • Late onset is typically sporadic
  • Early onset is typically familial (genetic)
17
Q

Define dementia.

A

A set of symptoms including memory loss, mood changes and problems with communicating and reasoning.

18
Q

What are the diagnostic criteria for dementia?

A
  • Multiple cognitive deficits (including amnesia)
  • Functional impairment
  • Clear consciousness
  • Change from previous level
  • Long duration (> 6 months)
19
Q

What are some standard neuropsychological tests for dementia?

A
  • MMSE - Mini-mental state examination. Maximum score 30. MCI < 27; AD < 25
  • ACE-R - Addenbrooke’s Cognitive Examination (revised): Includes MMSE, but more detail. Maximum score = 100, AD < 88
  • MOCA - Montreal Cognitive Assessment: Maximum score 30. HC = 25-29; MCI = 19-25; MD = 11-21
20
Q

What are some other disorders of ageing that may affect cognition?

A
  • Parkinson’s disease
  • Stroke
  • Depression
21
Q

What are some biomarkers for dementia?

A
22
Q

What are some risk factors and protective factors for cognitive decline (e.g. dementia and delirium)?

[IMPORTANT]

A
23
Q

What is the difference between dementia and delirium?

A
  • Both show forgetfulness, impaired memory, confusion and degrees of paranoia.
  • Dementia shows a progressive gradual decline.
  • Delirium shows a fluctuating course, sudden onset, with short duration, and impaired attention and awareness.
24
Q

Compare the causes of dementia and delirium.

[IMPORTANT]

A
  • Dementia -> Neurodegenerative, Vascular, etc.
  • Delirium -> Metabolic disturbances (e.g. hypoxia, hypoglycaemia, etc.), etc.

Both can be caused by toxins and infections.

25
Q

Is Alzheimer’s disease an inevitable part of ageing?

A
  • No
  • The threshold hypothesis (Roth, 1986) suggests that all aspects of AD pathology are seen to a lesser extent in normal aged individuals and that AD symptoms occur when normal ageing passes a threshold
  • However, this has been largely dismissed, since “By the age of 85 virtually everyone will have some neurofibrillary tangles in their cerebral cortex and yet not everyone develops AD.” (Smith, 2002)
26
Q

Compare the rate of thinning of the medial temporal lobe in Alzheimer’s disease and normal ageing. What is the signficance of this?

A

OPTIMA study found that:

  • The rate of medial temporal lobe thickness decline is up to 10 times greater in Alzheimer’s
  • This suggests that Alzheimer’s is a separate disease process and not just a normal part of ageing where AD happens once a threshold is reached