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Case 6 > Ageing and Cognition > Flashcards

Ageing and Cognition Flashcards

1
Q

What are the two methods for studying ageing

A

Longitudinal and cross-sectional

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2
Q

What is a longitudinal study

A

Recruitment of a representative sample tested repeatedly over time

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3
Q

What are the 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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4
Q

What are the disadvantages of longitudinal studies

A

Expensive, time consuming, high dropout rate (becoming less representative), practice effects (i.e. participants get better at the same test with repeated exposure)

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5
Q

What is a cross-sectional study

A

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

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6
Q

What are the advantages of cross-sectional studies

A

No re-testing, quicker and less expensive, lower dropout rates

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7
Q

What are the 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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8
Q

Describe cohort effects on memory

A

Flynn effect- substantial and sustained rise in IQ scores (fluid and crystallised intelligence) since 1932. Improvements in education (more people in secondary and tertiary education), nutrition and decrease in family size (parents focus resources on less children) over recent decades contribute to improved performance on memory tasks and IQ tests

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9
Q

What is one standard deviation in IQ

A

15

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10
Q

Account for the slightly different results in longitudinal and cross-sectional studies

A

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

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11
Q

What happens to short term memory

A

It progressively declines with age

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12
Q

What are there more pronounced ageing effects on

A

Tasks that require manipulation of information to be remembered

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13
Q

What happens to episodic memory through the adult years

A

It declines across the board: recall and recollection tests, verbal and visual materials, door and people test (people’s names and locations), memory for card hands, memorising passages, memory for conversations

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14
Q

What happens to semantic memory as you age

A

It does not decline, it actually expands in some areas

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15
Q

What happens to motor and perceptual performance with age

A

Declines, but older adults retain ability to learn implicit skills. Older adults take longer to acquire new skills but then their maintenance is the same as young adults

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16
Q

Describe the general mental slowing hypothesis

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 systems. Age-related sensory limitation (visual defects) and slowing of neural transmission thought to be responsible

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17
Q

Describe the common cause hypothesis

A

Sensory and cognitive functions correlated in older people, hand grip strength and cognition correlated in older people, slowed processing speed reflects a brain that it deteriorating in parallel with other bodily systems

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18
Q

Describe the inhibition deficit hypothesis

A

A major cognitive effect of ageing is the reduced capacity to inhibit relevant stimuli, linked with central executive component of working memory, reduced performance on Stroop task dual-tasking with increasing age in adulthood, ageing leads to mild “dysexecutive syndrome” like that seen after damage to frontal lobes. Mental slowing is die to degeneration of the nervous system

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19
Q

What happens to the overall brain as we age

A

Shrinks

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20
Q

What happens to the ventricles as we age

A

Expands

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21
Q

What happens to the frontal lobes as we age

A

Shrinks most rapidly

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22
Q

What happens to the temporal lobes as we age

A

Shrinks slowly

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23
Q

What happens to the hippocampus as we age

A

Shrinks slowly, then accelerates (possibly due to disease). Loses 20-30% of its neurons by age 80

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24
Q

What happens to the occipital lobes as we age

A

Shrinks slowly

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25
Q

What is dementia characterised by

A

A progressive deterioration of previously acquired intellectual abilities that interferes with social or occupational functioning

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26
Q

What are the risk factors for Alzheimer’s disease

A

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). A decrease in the concentration of glutamate plays a key role in Alzheimer’s

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27
Q

What is early onset of Alzheimer’s disease likely to be

A

Genetic

28
Q

What is the diagnostic criteria for Alzheimer’s disease

A

Multiple cognitive deficits in both (at least 6 months) memory (new information, previously learned info in severe cases) and one or more of the following cognitive abilities: language, action control, judgement, perception, executive function (planning and organising etc,). 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. Impairment in social function that represents a decline from previous levels, decline in emotional control or motivation. Gradual onset and continued cognitive decline. Deficits not due to other causes (cerebrovascular, Parkinson’s etc.)

29
Q

What are the key pathological changes observed at a cellular level in Alzheimer’s disease

A

Build-up on beta-amyloid peptide deposited extracellularly in plaques and tau protein (in pathological form) accumulating intracellularly as neurofibrillary tangles. Accompanied by neuronal loss, pathological diagnosis of AD rests on presence of amyloid plaques and NFT

30
Q

Explain how anterograde amnesia is a clincal hallmark of Alzheimer’s disease

A

Complaints of memory difficulty by far the commonest symptom noticed by patients and particularly by their family (informants). Report that the person repeats questions; forgets appointments; misplaces car keys; forgot items on a shopping list; forgets recent events of interest (e.g. football team’s results). By the time AD has been reliably diagnosed, patients are likely to show a 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.).

31
Q

What is anterograde amnesia

A

When older adults struggle to take new information on (very common in AD)

32
Q

What is poor performance in declarative memory a powerful indicator of

A

You going on to develop Alzheimer’s disease

33
Q

How does Alzheimer’s disease relate to semantic memory

A

Mildly demented AD patients often also impaired on tests of semantic memory (memory for facts), naming (e.g. famous faces, buildings, familiar objects), verbal fluency (e.g. by generating list of animals), generation of word definitions and matching words to pictures. Typically occurs at a later stage and to a more modest extent than to episodic memory. The more progresses AD the more you struggle to name an object described (semantic memory)

34
Q

Describe the effect of Alzheimer’s disease on working memory

A

Impairment less marked than declarative memory. Working memory deficit initially mild, primarily involves disruption of the central executive with relative sparing of immediate memory

35
Q

Describe the effect of AD on simple span

A

Generally spared (STM), impaired on complex attention task dependent upon effective allocation of attentional resources (e.g. dual-processing tasks)

36
Q

Describe the effect of AD on implicit memory

A

Improve at the same rate as controls on motor and cognitive skill learning tasks (e.g. mirror tracing, reading mirror-reversed words)

37
Q

What is the best predictor of declarative memory in Alzheimer’s disease

A

Hippocampal atrophy

38
Q

Describe AD progression

A

Striking impairment in declarative memory now considered to be cognitive hallmark of AD, thought to result from pathological alternations (e.g. NFTs neurofibrillary tangles) seen in MTL (medial temporal lobe) regions early in disease. Only as pathology spreads to other neocortical regions do additional cognitive symptoms emerge and full dementia becomes apparent

39
Q

What impact does decrease in hippocampal volume have

A

The more significant decrease in volume of the hippocampus the worse episodic memory is

40
Q

What is mild cognitive impairment (MCI)

A

Intermediate cognitive state where patients are neither cognitively intact nor demented

41
Q

Describe the amnestic of MCI

A

Clinically significant memory impairment that does not meet the criteria for dementia. Typically, patients & their families aware of increasing forgetfulness. However, other cognitive capacities, e.g. executive function, use of language, visuospatial skills, are relatively preserved

42
Q

Describe the role of longitudinal studies in exploring if some individuals with MCI have early Alzheimer’s disease

A

Declarative memory (e.g. free recall) performance significantly worse among individuals with MCI who subsequently receive a diagnosis of AD on followup, as compared with those who also report memory problems but do not progress to dementia within a few years. On average, 3 years prior to the diagnosis of amnestic MCI and 6 years prior to the diagnosis of probable AD, subjects who are predestined to become demented already show specific disease-associated changes focused on the hippocampus

43
Q

Describe anterior regions of the brain

A

Greater white matter tract vulnerability

44
Q

What happens in normal neurocognitive ageing

A

Frontal lobes shrink and there is a decrease in the neurotransmitter dopamine

45
Q

What impact does frontal lobes shrinking have

A

Decrease in processing and decrease in central executive

46
Q

Explain the two component view of neurocognitive ageing

A

Component 1: impaired function of prefrontal cortex. Component 2: Disruption of the medial temporal lobe memory system (including hippocampus) leads directly to episodic LTM impairement

47
Q

Describe how impaired function of prefrontal cortex occurs

A

Loss of grey matter volume; reduced integrity of frontal working memory tracts; reduced levels of neurotransmitters (especially dopamine)

48
Q

What are frontal cortical changes suggested to be a component of

A

Normal ageing

49
Q

Who are changes in prefrontal cortex observed in

A

Individuals without dementia symptoms or hypertensive illness; develop gradually throughout adulthood, show a linear decline +5% per decade from age 20; correlate with age-related declines in processing speed central executive component working memory (e.g. ability to inhibit irrelevant information)

50
Q

Describe changes that lead to disruption of the medial temporal lobe memory system (including hippocampus) leads directly to episodic LTM impairment

A

Hippocampal volume reduction with ageing is curvilinear- accelerated 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 ageing

51
Q

What are medial temporal changes suggested to be a consequence of

A

Pathological ageing

52
Q

What is the role of smoking in non-pathological ageing

A

Poorer cognitive ageing

53
Q

What is the role of diet and nutrition in non-pathological ageing

A

Mediterranean diet might be protective

54
Q

What is the role of activity and participation in physical fitness in non-pathological ageing

A

Active and engaged lifestyle seen as beneficial for later cognitive function

55
Q

What is the role of participation in activities of an intellectually stimulating nature in non-pathological ageing

A

Predict reduced cognitive decline ‘use it or lose it’

56
Q

What is the role of cardiovascualr disease and its risk factors in non-pathological ageing

A

Individuals with poorer physical health status experience greater cognitive decline

57
Q

What is the role of education and social class in non-pathological ageing

A

More years spent in formal education and higher social class are associated with less cognitive decline

58
Q

What are problems of reverse causation

A

Individual differences in cognitive ability in old age reflect two things- differences in prior cognitive ability and differences in the degree to which change (typically deterioration) has taken place

59
Q

What does childhood cognitive ability predict

A

Later diet choices, educational attainment, social status, choice of leisure pursuits, health habits etc. and account for links between these factors and late life cognitive health. Early life cognitive ability is the strongest predictor of late-life non-pathological cognitive ageing

60
Q

What are a risk factor of pathological cognitive ageing

A

Lower levels of education and social class

61
Q

What does disruption to medial temporal lobe memory system lead directly to

A

Declarative memory impairment

62
Q

What may frontal system changes underlie

A

Reduced processing speed and mild working memory difficulties in ‘normal’ ageing

63
Q

A 72-year-old male presents to a memory clinic with his son who is concerned over his father’s forgetfulness. He scores 19 on the MoCA, has difficulty recalling recent events and exhibits impairment in declarative memory. Which region is most likely primarily affected by this ‘type’ of ageing

A

Medial temporal lobe. A deficit in declarative memory, supported by a MoCA score of 19 or below in addition to anterograde amnesia suggests pathological ageing which is associated with changes in the medial temporal lobe

64
Q

An 81-year-old female completes a cognitive assessment task that reveals reduced processing speed and decline in executive working memory performance (i.e. attention planning, cognitive control). Declarative memory, specifically semantic, remains unaffected. What region is most likely responsible for these changes

A

Prefrontal cortex. Decline in executive function and processing speed are part of the normal ageing process and are associated with changes to the prefrontal cortex

65
Q

A team of researchers investigated how well a group of participants in their 70s were able to perform certain future tasks. They revealed that older adults tend to use various strategies, such as keeping diaries, to remember future events. What type of memory were they assessing

A

Prospective. Prospective memory refers to the ability to plan, retain and retrieve information relating to an action to intention to be performed at some point in the future (remembering to remember). It relies on working memory and retrospective memory (i.e. episodic) but may also involve separate processes independent of these

Case 6 (10 decks)

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