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Why We Remember & Forget > L8 - Memory, Aging and Dementia > Flashcards

L8 - Memory, Aging and Dementia Flashcards

1
Q

Impaired memory is the earliest and best predictor of what?

A

The onset of Alzheimer’s

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2
Q

How would longitudinal studies typically measure changes in memory with age?

A

The same group of individuals would be tested on their memory at the start of the study, and then again a number of years later, and then again a number of years after that (e.g. 0 years, 10 years, 20 years).

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3
Q

How would cross-sectional studies typically measure changes in memory with age?

A

At the start of the study, a group of a particular age would be tested (i.e. 20 year olds). 10 years on, a different group of 30 year olds would be tested, and then 10 years from that a group of 40 year olds would be tested.

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4
Q

What are the advantages of using longitudinal studies to measure memory and aging?

A

+ Effect of age can be determined on an individual basis, helping to pinpoint precursors of a disease.

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5
Q

What are the limitations of using longitudinal studies to measure memory and aging?

A
  • Expensive and time consuming
  • High dropout rate
  • Practice effects
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6
Q

What are the advantages of using cross-sectional studies to measure memory and aging?

A

+ No re-testing, so lower drop-out rate and no practice effects
+ Quicker and less expensive

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7
Q

What are the limitations of using cross-sectional studies to measure memory and aging?

A
  • No direct comparison, performance can’t be related to past/future data
  • Insensitive to cohort effects
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8
Q

What did Deary et al., (2004; 2006) find about the correlation between early and elderly IQ?

A

Early IQ at 11 years was highly correlated with IQ at 80 years (r = .66).

IQ at 11 was a good predictor of physical fitness at 80.

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9
Q

What are the general findings on performance changes in aging with tests of verbal memory span?

A

Elderly remember less than 1 fewer item.

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10
Q

What are the general findings on performance changes in aging with tests of visual memory span?

A

Less than 1/2 an item

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11
Q

What are the general findings on performance changes in aging with tests of verbal working memory?

A

Modest decline in recalling words in alphabetical order

Only a small decline in sentence span

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12
Q

What did May et al., (1999) propose about the reasons for impaired memory in the elderly?

A

A buildup of proactive interference - perhaps older adults are less able to inhibit interference from older memories.

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13
Q

What is the inhibition deficit hypothesis of aging?

A

Proposes that many of the observed changes in memory performance result from the inability to inhibit irrelevant information, not necessarily from memory deficits themselves.

Therefore, memory dysfunction may result from attention deficits, or impaired ability to allocate resources.

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14
Q

How does episodic memory change throughout adulthood?

A

Declines steadily, across different tests. Some tasks are more problematic than others

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15
Q

What are the two features proposed by Craik (2005) to modulate decline in episodic memory?

A
  • processing capacity of the learner (elderly take longer to perceive materials, and are less likely to develop and use complex learning strategies)
  • level of environmental support provided during retrieval (age effects are largest in tests lacking external cues)
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16
Q

What did Naveh-Benjamin (2000) find about semantically related or unrelated word pairs in young and old participants?

A

Elderly participants showed impaired memory for unrelated but not related words, more so during cued free recall than during recognition.

Therefore, the elderly seem to be less able to form associative links

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17
Q

What did Naveh-Benjamin (2003) find about attentional resources in the young, and its effect on memory performance for semantically related and unrelated words?

A

Used a secondary task to occupy cognitive resources.

This impaired memory equally for both related and unrelated word items.

Therefore, differences in memory performance between young and old are attributable to learning capacity, rather than attentional differences.

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18
Q

What is the associative deficit hypothesis of aging?

A

Proposes that the age deficit in memory comes from an impaired capacity to form associations between previously unrelated stimuli

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19
Q

What did Naveh-Benjamin (2004b) study to test the associative deficit hypothesis?

A

Recognition tests for names, faces, or their association. Tested groups of young, elderly and young with divided attention.

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20
Q

What did Naveh-Benjamin (2004b) find when testing the associative deficit hypothesis?

A

Elderly showed a specific impairment on the name-faces association, even when attentional differences were controlled for.

–> supports the associative deficit hypothesis

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21
Q

What is prospective memory?

A

Remembering to carry out future actions

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22
Q

Prospective memory has been partly shown to involve the same mechanisms as what?

A

Episodic memory

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23
Q

What do laboratory studies show about prospective memory differences between young and old participants?

A

Show that older participants have a deficit in prospective memory

  • Mantyla and Nilsson (1997) asked participants to sign a form at the end of the session. 61% of young subjects (35-45 years) remembered to, but only 25% of older subjects did (70-80 years old).
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24
Q

What are the real life differences in prospective memory, if any, between young and old individuals?

A

Differences in the lab but not in tasks embedded into real life.

Rendell & Thomas (1999) asked PPS to complete tasks in the lab or in real life, in groups of 20, 60 or 80 year olds.

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25
Q

What are the possible explanations for why differences in prospective memory exist between young and old people in the lab, but not in real life?

A

Elderly use diaries to compensate for prospective memory lapses, have more structured/consistent days,

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26
Q

What are the differences in semantic memory in old age?

A

Semantic memory actually increases, but the speed of memory selection/access for semantics is impaired - this has been attributed to language and processing deficits

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27
Q

How do older people write differently to young people?

A

Construct sentences more concisely - less unnecessary words. Write in a way that seems to use working memory less (Kemper, 1990)

28
Q

Wht are the differences in implicit learning between old and young people?

A

Results are mixed due to the differences in implicit memory tests:

Moderate impairments with priming tasks involving response production in the elderly.

Small/no impairments with classification tasks, such as lexical decision-making.

29
Q

What is the false fame effect?

A

Older people are more likely to trust familiar information or people, than young people would.

This can increase their susceptibility to leading questions, etc

30
Q

How is motor skill different in older ages?

A

Motor performance declines with age. Speed of execution is slower, but rate of learning is intact.

31
Q

What can lead to resistance of age effects?

A

Good physical health (diet, and regular exercise)

32
Q

How do rates of memory decline differ between professors and blue-collar (construction) workers?

A

They don’t - as long as the brain is active, age effects are resisted (Christensen et al., 1997).

33
Q

How does active learning when older help to protect against age effects?

A

Meaningful material may allow the active learner to compensate for declining episodic memory (Shimamura et al. 1995).

34
Q

What is the main limitation typically found with memory training programs?

A

They are found not to generalise to other cognitive domains that the training doesn’t target. They may provide protective effects, but doesn’t provide a boost in all-round cognitive performance.

35
Q

What do Salthouse and Becker (1998) suggest about the independence of memory decline?

A

Argue that there is no single factor for memory decline which is separate from general cognitive decline.

36
Q

What did Gazzaley et al., (2010) show about the inhibition deficit hypothesis?

A

Told young and old people to either remember the scene in the image, passively look at it, or ignore it.

They found that parahippocampal activity was greatest for the remember conditions in both age groups, lesser for passive conditions in both age groups, but even less for ignore conditions, only for younger participants. For older participants, activation was the same in the passive and ignore conditions, suggesting they were unable to inhibit processing activity when the information was irrelevant.

  • this supports the inhibition deficit hypothesis, at least in the context of working memory
37
Q

How might frontal lobe deficits explain cognitive impairments with age?

A

Frontal lobes lose more and more cells with age (atrophy). These regions are crucial for working memory, and attention. Therefore, memory tasks which rely on both of these processes are likely to be impaired if the frontal lobe has less contributing activity.

38
Q

Can frontal lobe deficits explain cognitive impairments with age?

A

Not massively. The correlation between frontal lobe atrophy and age-related cognitive decline is weak, and the theory is not well supported at the current moment.

39
Q

As we age, the whole brain _____?

A

As we age, the whole brain shrinks

40
Q

As we age, the ventricles _____?

A

As we age, the ventricles expand

41
Q

As we age, the frontal lobe _____ ______ _____?

A

As we age, the frontal lobe shrinks most rapidly

42
Q

As we age, the temporal lobe _____ _____?

A

As we age, the temporal lobe shrinks slowly

43
Q

As we age, how does the hippocampus change in size?

A

At first, it shrinks slowly, but then later losses accelerate (possibly due to disease)

20-30% of cells in the hippocampus are lost by age 80.

44
Q

As we age, the occipital lobe ____ _____?

A

As we age, the occipital lobe shrinks slowly

45
Q

What do neuroimaging studies reveal about differences in the aging brain?

A
  • Broader activations: bilateral activation for WM and visual attention tasks in the elderly, but not in the young (Cabeza et al., 2004), and bilateral hippocampal activation on autobiographical memory tasks (Maguire & Frith, 2003) - suggests older people are having to recruit more of the brain to perform to the same level as younger people
  • reduced activation in the elderly: older people do not show activation in occipito-temporal areas, that young people do, in a complex visual memory task (Lidaka et al., 2001). –> elderly seem to rely on more simple strategies on complex tasks.
46
Q

What is the role of dopamine in memory?

A

Dopamine plays a specific role in novelty and reward processing, which are both known to increase plasticity in the hippocampus

47
Q

How can we be sure that dopamine influences memory?

A

Dopamine agonists improve spatial working memory, while dopamine antagonists impair spatial working memory.

Evidence such as this shows, in almost a double dissociation, that changes in dopamine transmission can impact on performance when working memory is necessary.

48
Q

What is the primary feature of Alzheimer’s disease (AD)?

A

Defective episodic memory (Peterson et al., 2001)

49
Q

What are the warning signs of AD?

A 
Memory loss affecting job skills
Difficulty performing familiar tasks
Language problems
Disorientation in time and space
Poor judgement
Change in personality
Changes in mood
Loss of initiative
50
Q

Describe the prevalence of AD

A
  • Accounts for over 50% of senile Dementia cases.
  • Occurs in 10% of the population over age 65
  • The rate of occurrence increases with age
51
Q

What is the diagnostic criteria for AD, according to the DSM-V?

A

Memory impairment + 2 or more deficits in cognitive function (i.e. language processing, action control, perception or executive function)

52
Q

What does MCI stand for?

A

Mild Cognitive Impairment

53
Q

What is MCI characterised by?

A

Measurable memory impairment, greater than those typically expected with aging, but not severe enough to interfere with daily life.

It is a transitional state between healthy aging and dementia

54
Q

What are beta amyloid plaques?

A

Neurotoxic clumps of amyloid created by faulty protein division.

55
Q

What are neurofibrillary tangles?

A

Formation of abnormal proteins within neurons. Results in twisting of microtubules, and eventually cell death.

56
Q

What does an ultimate diagnosis of AD typically require?

A

A post-mortem finding of dense beta amyloid plaques and neurofibrillary tangles

57
Q

What is the typical neural progression of AD?

A

Starts in the hippocampus - cell death.

Then spreads to temporal, parietal and then frontal lobes.

58
Q

What is unique in classifying healthy controls and MCI patients?

A

Hippocampus volume

59
Q

What is the main difference in neural progression between MCI and AD?

A

MCI doesn’t extend to the cortex itself but AD does.

60
Q

What did Garrard et al., (2005) find about the progression of AD in Novelist and Philosopher, Iris Murdoch?

A

Linguistic problems as the disease progressed:

  • difficulty coming up with certain words
  • spelling deteriorated
  • sentences became shorter and used lower-frequency words (potentially a compensatory strategy)
  • semantic difficulties: major problems in defining words, naming pictures became difficult, and problems generating items from a semantic category.
61
Q

Describe the episodic memory impairments in AD.

A

Deficits in:

  • recall
  • recognition
  • verbal materials
  • visual materials
  • everyday memory
62
Q

Is the recency and primacy effect preserved in AD patients?

A

Recency is relatively preserved until later stages, in which both effects are removed.

63
Q

Compare the rate of forgetting between AD patients and controls.

A

Rate of forgetting information is the same between AD patients and controls

64
Q

Hodges, Patterson and Tyler (1994) found what about atrophy in areas of the brain that relate to semantic memory deficits in AD patients.

A

Atrophy in temporal regions can predict impairments on semantic memory

65
Q

Describe the extent of impairment on implicit memory (priming, motor skill and skill learning) in AD patients

A

Priming is intact in AD patients as long as it requires a shallow level of processing (Beauregard et al., 2001).

Worse to begin with on motor skill tasks, but show a normal pattern later on (Heindel et al., 1989).

Very small impairment in improvement rate for AD patients on skill learning (i.e. mirror reading) - Moscovitch, (1982).

66
Q

How is working memory affected by AD?

A

Working memory is not as impaired as episodic memory, but there are still modest deficits in digit span and corsi block tapping (visuo-spatial WM)

AD patients can maintain small amounts of information over unfilled delays, as long as they are able to use their phonological loop to rehearse. Articulatory suppression causes rapid forgetting.

67
Q

What are AD treatments focused on?

A

Treatments are about breaking down enzymes, tog et more Acetylcholine building up in the brain, which slows down the disease progression (Ach depletion)

Nothing can be done to cure, only to slow progression and improve quality of life.

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