Memory and Ageing Flashcards

1
Q

Age-related changes to cognition aren’t entirely due to primary biological ageing processes, also due to:

A

*Environmental factors (early and present)
*Lifestyle factors
*Systemic disease

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2
Q

Two methods for studying ageing:

A

*Longitudinal studies
*Cross-sectional studies

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3
Q

what is a longitudinal study

A

Recruitment of a representative sample tested repeatedly over time

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4
Q

what is a cross-sectional study

A

Recruitment of different groups of people sampled across the age range, with each being tested once and only once

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5
Q

advantages of longitudinal studies

A
  • Effect of age can be determined on an individual basis ->useful in pinpointing precursors of disease
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6
Q

disadvantages of longitudinal studies

A
  • Expensive
  • Time consuming
  • High dropout rate (becoming less representative)
  • Practice effects
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7
Q

advantages of cross-sectional studies

A
  • No re-testing
  • Quicker and less expensive
  • Lower dropout rates
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8
Q

disadvantages of cross-sectional studies

A
  • Performance can’t be related to individual earlier/future performance
  • Cohort effects (i.e. people born at different times differ due to changes in diet,
    education, social factors, family size, etc.
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9
Q

Flynn effect

A

[* Substantial and sustained rise in IQ scores
(fluid & crystallised intelligence) since 1932]

  • Improvements in education, nutrition, and
    decrease in family size over recent
    decades contribute to improved
    performance on memory tasks and IQ tests
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10
Q

how may longitudinal studies and cross-sectional studies differ in results

A

Longitudinal studies might underestimate age- related changes (e.g. practice effects); cross- sectional studies might overestimate them (e.g. cohort effects)

[* Important to consider education in accounting for cognitive level, and to adjust accordingly to address practice and cohort effects]

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11
Q

*More pronounced ageing effects on tasks that require?

A

that require manipulation of information to be remembered

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12
Q

example test of verbal span

A

digit span

general findings: declines by <1 item

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13
Q

example test of visual span

A

corsi block tapping

general findings: declines by < 1/2 an item

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14
Q

example test of verbal working memory

A

recalling words in alphabetical order - modest decline
sentence span - small decline

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15
Q

the magnitude of decline of episodic memory depends on?

A

depends on the nature of the task and the
method of testing (free recall is more impaired than recognition)

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16
Q

does semantic memory decline with age?

A

no, it actually expands with age in some areas:
* Vocabulary
* Historical facts

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17
Q

does Motor and perceptual performance decline with age?

A

yes

[Speed of perception and movement become
impaired. But older adults retain ability to learn and retain new implicit
skills]

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18
Q

What are the hypotheses regarding the
causes of age related cognitive decline - General mental slowing hypothesis (Salthouse, 1996)

A
  • Many of the cognitive effects of ageing are caused by reduced processing speed [the rate at which tasks can be performed, due to ageing nervous system]
  • Age-related sensory limitation (visual deficits) and slowing of neural transmission is thought to be responsible
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19
Q

What are the hypotheses regarding the
causes of age related cognitive decline - “Common cause hypothesis”
(Baltes & Lindenberger, 1994, 1997)

A
  • Sensory and cognitive functions are correlated in older people
  • Hand grip strength and cognition correlated in older people
  • Slowed processing speed reflects a brain that is deteriorating in parallel with other bodily systems
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20
Q

A major cognitive effect of ageing is?

A

the reduced capacity to inhibit irrelevant stimuli
* Linked with central executive component of
working memory
* Ageing leads to a mild “dysexecutive
syndrome” like that seen after damage to
frontal lobes

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21
Q

Age effects on declarative long-term memory
resemble what?

A

resemble a mild anterograde amnesia and
are separable from either processing speed
or working memory

22
Q

multiple factors contribute to age effects on cognition, some of which are consequences of ____ and others which are consequences of ____

A

some of which are consequences of normal ageing, others of which are consequences of disease processes

23
Q

Risk & protective factors in non- pathological
cognitive ageing - name 2

A

Smoking – linked to poorer cognitive health
Diet & nutrition – ‘Mediterranean diet’ might be protective
Activity participation and physical fitness - active and engaged lifestyles seen as beneficial for later cognitive function
Participation in activities of an intellectually stimulating nature - predict reduced cognitive decline: ‘use it or lose it’
Cardiovascular disease and its risk factors – Individuals with poorer physical health status experience greater cognitive decline
Education and social class - More years spent in formal education and higher social class are associated with less cognitive decline

24
Q

Individual differences in cognitive ability in old age reflect two things:

A
  • Differences in prior cognitive ability
  • Differences in the degree to which change (typically deterioration) has taken place
25
what is the strongest predictor of late-life non-pathological cognitive ageing
Early life cognitive ability
26
as we age, what happens to overall brain
overall brain shrinks
27
as we age, what happens to ventricles in the brain
expands
28
as we age, what happens to frontal lobes
Shrinks most rapidly
29
as we age, what happens to temporal lobes
Shrinks slowly
30
as we age, what happens to hippocampus
Shrinks slowly, then accelerates (possibly due to disease) [Loses 20–30% of its neurons by age 80]
31
as we age, what happens to occipital lobes
Shrinks slowly
32
Differential effects of ageing on specific brain regions supports a two-component view of ageing - component 1: Impaired function of prefrontal cortex
Loss of grey matter volume; reduced integrity of frontal white matter tracts; reduced levels of neurotransmitters (especially dopamine) These changes: * Are observed even in individuals without dementia symptoms or hypertensive illness * Develop gradually throughout adulthood, (shows a linear decline from age 20) * Correlate with age-related declines in processing speed, central executive component working memory (e.g. ability to inhibit irrelevant information) Frontal cortical changes are a component of ‘normal’ ageing
33
Differential effects of ageing on specific brain regions supports a two-component view of ageing - component 2: Disruption of the medial temporal lobe memory system (inc. hippocampus) leads directly to episodic LTM impairment
Hippocampal volume reduction with ageing: * Is curvilinear – accelerating rapidly after ± age 70 * Is unrelated to cognitive function over most of adult lifespan; however after ± age 60 hippocampal volume predicts explicit memory performance * Is predicted by family history of Alzheimer disease * Is absent in individuals age 90+ who do not show Alzheimer’s disease pathology – i.e. not an inevitable consequence of aging Medial temporal lobe changes might be a consequence of pathological ageing
34
Dementia is defined as a syndrome characterised by?
a progressive deterioration of previously acquired intellectual abilities that interferes with social or occupational functioning
35
risk factors of Alzheimer's Disease (AD) - name 2
Age is the strongest risk factor for AD (but AD is not an inevitable component of ageing) Genetics * Family history of AD * Specific risk genes (APOE-ε4) Medical history * Vascular disease * Depression Life events * Lifestyle factors (poor health habits, e.g. smoking, overweight, etc.) * Head injury (dementia pugilistica in boxers)
36
Diagnostic criteria for Alzheimer’s disease: ICD-11. Name 3
Significant decline in cognitive abilities, affecting at least two cognitive domains, including: Two or more of the following cognitive abilities: * Memory, language, action control, social cognition and judgement, perception, executive function, attention, psychomotor speed, visuospatial or visuo-perceptual abilities Preserved awareness of environment (absence of clouding of consciousness) for a period of time allowing confirmation of above deficits not due to superimposed episode of delirium Functional impairment: the cognitive impairment must be severe enough to interfere with an individual’s ability to perform activities of daily living and maintain independence Gradual onset and continued cognitive decline Deficits not due to other causes (cerebrovascular, Parkinson’s, etc.)
37
Key pathological changes observed in Alzheimer’s disease brain tissue
At cellular level, AD associated with build up of: * Beta-amyloid (Aβ) peptide – deposited extracellularly in plaques * Tau protein (in a pathological form), accumulating intracellularly as neurofibrillary tangles (NFT) * Accompanied by neuronal loss * Pathological diagnosis of AD rests on presence of amyloid plaques and NFT
38
Anterograde amnesia: clinical hallmark of Alzheimer’s disease. name 2 things of anterograde amnesia seen in AD patients
Complaints of memory difficulty by far the commonest symptom noticed by patients, and more particularly by their family (informants) person repeats questions; forgets appointments; misplaces car keys; forgets items on a shopping list, forgets recent events of interest (e.g. football team’s results)
39
By the time AD has been reliably diagnosed, patients are likely to show a substantial deficit in?
substantial deficit in declarative memory using a variety of cognitive procedures (e.g. free recall, recognition, paired- associates learning) and across modalities (visual, auditory, etc.
40
what about semantic memory in Alzheimer's Disease?
Mildly demented AD patients often also have impaired semantic memory on tests, such as (memory for facts): * Naming (e.g. famous faces, buildings, familiar objects) * Verbal fluency (e.g. generating list of animals) * Generation of word definitions; matching words to pictures Typically occurs at a later stage and to a more modest extent than episodic memory impairment
41
In AD, working memory is more or less impaired than declarative memory?
working memory is less severely affected than declarative memory
42
how does working memory deteriorate in AD?
Working memory impairment is initially mild, primarily involves disruption of the central executive with relative sparing of immediate memory *Simple span is generally spared (short-term memory), impaired on complex attention tasks
43
what happens to implicit memory in AD?
Implicit memory can still improve at the same rate as people without AD on motor and cognitive skill learning tasks (e.g mirror tracing)
44
2 bullet points on Alzheimer’s disease progression (speak of a hallmark and pathology)
cognitive hallmark of AD is Striking impairment in declarative memory. this is thought to result from pathological alterations (e.g. NFTs) seen in medial temporal lobes regions early in disease Only as pathology spreads to other neocortical regions do additional cognitive symptoms emerge and full dementia syndrome becomes apparent
45
what is consistently the best predictor of declarative memory impairment in Alzheimer disease
Hippocampal atrophy
46
Distributed neocortical atrophy predicts what in AD?
semantic impairment (e.g. animal fluency)
47
what is Mild cognitive impairment (MCI)
intermediate cognitive state where patients are neither cognitively intact nor demented
48
what is Amnestic MCI
Amnestic MCI: clinically significant memory impairment that does not meet the criteria for dementia.
49
5 criteria of MCI
1) memory complaint, preferably qualified by an informant (e.g family) 2) memory impairment for their age 3) preserved general cognitive function 4) Intact activities of daily living 5) Not demented (not dementia)
50
Do some individuals with MCI have early Alzheimer disease?
Longitudinal studies have shown: Declarative memory (e.g. free recall) performance is significantly worse among people with MCI who later receive a diagnosis of AD, as compared with those who also report memory problems but do not progress to dementia within a few years
51
Frontal systems changes may underlie?
reduced processing speed and mild working memory difficulties in ‘normal’ ageing