w2: Ageing II Flashcards

1
Q

How do we study the ageing brain?

A

-post-mortem (problem- low sample size)
- neuroimaging techniques (CT, MRI, fMRI, PET)

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2
Q

changes in the human brain

A
  • weight of brain decreases up to 10%
  • weight of brain relative to body weight stays relativelly stable from age 20+
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3
Q

changes in human brain: ageing

Brain Volume

A

Cerebral cortex as a whole decline:
- 0.12% per year in younger adults.
- 0.35% per year in adults over 53 years of age.
Strong differences between regions:
- Some show a relatively steep decline.
- Others have a relatively stable volume over time.

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4
Q

changes in human brain: ageing

Grey Matter

brain areas that reduce and stay stable in size

A

Brain regions that reduce in volume with age:
- Caudate nucleus.
- Lateral prefrontal cortex.
- Cerebellar hemispheres
- Hippocampus.

Brain regions with minimal reduction or stable volume with age:
- Primary visual cortex
- Entorhinal cortex

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5
Q

Age related atrophy of grey matter differs across regions.

A
  • The frontal lobes show the most atrophy. Between 0.9% and 1.5% per year.
  • The parietal lobes show the second most atrophy per year. 0.34% and 0.9% per year.

Decline becomes steeper with increasing age.
Example: hippocampus.
- 0.86% per year in whole sample.
- 1.85% per year after the age of 70.

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6
Q

changes human brain: ageing

white matter

A

Throughout the entire brain
Greatest while matter loss in frontal regions.
- White matter loss is more extensive than grey matter loss.

Anterior to posterior gradient (from front of brain to the back of brain- ie. down hairline)

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7
Q

changes in brain: ageing

brain cavity and CSF

A

Between ages of 20 and 50 the brain occupies 90% of the cranial cavity.
Thereafter: the brain occupies progressively less space.
- Increase in the volume of cerebrospinal fluid.
- Widening of the sulci.

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8
Q

changes during ageing

Neurotransmitters

in case of dopamine

A

Two main families of dopamine receptors
- D1
- D2

Aging: loss of D1 and D2 receptor binding
- Decrease 7-10% per decade.

Dopamine transporter.
- 4.4% to 8% per decade.

Anterior-posterior gradient.

Neurotransmitter: loss of receptors and transporters

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9
Q

are the structural changes of influence on cognition?

A

yes!
significant correlation b/w decline in brain structure and cognitive functioning.

  • Representations are generally well maintained at older ages, but some knowledge is either lost (especially with lack of practice) or becomes inaccessible.
  • Control processes develop at different ages and also decline differentially, depending in part on the brain areas involved.
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10
Q

which domains decline

Ageing and Cognitive Decline

A

significantly decline
- speed of processing
- Working Memory
- LTM
- STM- but less than ^^

verbal knowledge = intact, increases for some people.

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11
Q

Functional Challenges in the brain

A
  • Neuronal activity associated with cognition shows both age-related decreases as well as increases.
  • Young adults and older adults (partly) recruit different areas of the brain for the same tasks.

Refer to age related:
- Compensation
- Adaptation

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12
Q

Age-related functional activations

pattern 1

Posterior-Anterior shift ageing (PASA)

A

PASA refers to a functional shift in brain activity from posterior (back) regions to anterior (front) regions with increasing age.

decreased activation in **posterior regions **(e.g., occipital and parietal lobes), which are typically involved in sensory and perceptual processing.

increase in activation in **anterior regions **(e.g., prefrontal cortex), which are involved in executive functions like planning, decision-making, and working memory.

shift = compensatory mechanism, old brains recruit frontal regions to compensate for decline in sensory + cognitive processing.

PASA suggests that ageing is accompanied by a redistribution of brain activity, reflecting attempts to maintain cognitive function

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13
Q

Age-related functional activations

pattern 2

Hemispheric Asymmetry Reduction in Older Adults
(HAROLD)

A

HAROLD describes a reduction in the typical functional asymmetry of brain activity in older adults, where tasks that usually activate one hemisphere begin to engage both hemispheres.

young adults, cognitive tasks ie. memory = laterised activity
older adults, same task = bilateral

bilateral activation is thought to compensate for declining efficiency in one hemisphere by engaging the corresponding regions in the opposite hemisphere.

  • HAROLD reflects the brain’s capacity to reorganise itself to counteract age-related decline, particularly in tasks requiring memory, language, and attention.
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14
Q

explainations PASA+ HAROLD

compensation + dedifferentiation account

A
  1. Compensation: bilateral activity is associated with successful cognitive performance. Found in high-performing rather than low-performing older adults.
    2.** Dedifferentiation account: **more widespread activation reflects an age-related difficulty in engaging specialised neural mechanisms.
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15
Q

cognitive ageing theories

Sensory Deficit Theory

A

Age-related deficits in sensory processing play a major role in age-related cognitive decline.
Older adults show considerable deficits in:
- Visual processing
- Auditory processing

Strong correlations between age-related differences in sensory processing and cognitive performance

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16
Q

cognitive ageing theories

Resource Deficit Theory

A

**Aging is associated with a reduction in the amount of attentional resources
- Result: deficit in demanding cognitive tasks **
- Deficits are smaller when environment provides support

Support: when attentional resources are reduced in younger adults, they tend to show cognitive deficits that resemble those of older adults.

Also support from neuroimaging studies:
- *Attention relies strongly on the prefrontal cortex (PFC)

Older adults tend to show decreased activation in a part of PFc that is activated during attention tasks in young adults*.
Older adults tend to shoe a more bilateral pattern of PFC activity during attention tasks.

 HAROLD

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17
Q

cognitive ageing theories

Speed Deficit Theory

A

speed processing = refers to how quickly the brain can encode, interpret, and respond to information.
With age, the brain’s neural pathways and communication efficiency decline, leading to slower processing.

slowing of processing speed impacts other cognitive domains such as memory, problem-solving, and reasoning.

Limited Time Mechanism:

Because processing speed is slower, older adults may not have enough time to complete all the necessary mental operations before new information is presented or before they must respond.
Simultaneity Mechanism:

As processing takes longer, it becomes harder for older adults to hold earlier steps of a task in working memory while engaging in subsequent steps. This impacts their ability to integrate information effectively.

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18
Q

mechanisms speed deficit theory

A

White Matter Deterioration:

The myelin sheath, which insulates axons and facilitates fast signal transmission between neurons, deteriorates with age.
This deterioration reduces the speed and efficiency of neural communication, particularly in areas of the brain associated with complex cognitive tasks.

Increased Neural Network Demand:

As the brain ages, it compensates for declining efficiency in certain areas by recruiting additional neural networks to support cognitive performance.
This compensatory mechanism often increases cognitive load and slows down overall processing speed because it requires additional time and resources for task execution.

19
Q

cognitive ageing theories

Inhibitory Deficit Theory

A

Age-related cognitive decline is due to a decline in the inhibitory control of working memory contents.
- When inhibitory control fails, goal-irrelevant information gains access to working memory.
- Result: mental clutter, which impairs working memory

Support: older adults
- Better remember disconfirmed solutions
- Better remember to-be-forgotten information
-Older adults show weaker activity than younger adults in inhibitory control regions
- Older adults show **greater activity in regions that are supposed to be inhibited than younger adults. **

20
Q

model that combines it all

Scaffolding Theory of Ageing and Cognition (STAC model)

A

STAC model: accounts for the possibility of both deficient and preserved performance on cognitive tasks:
- Acknowledge that the aging brain must adapt to neural challenges including atrophy
- To cope: the brain builds alternative neural circuitry, or scaffolds
- Scaffolds: represent compensatory strategies and allow older adults to maintain a high level of activation.

Model is not specific to old age, but to the life span the brain is confronted with cognitive challenges.

21
Q

Cognitive Reserve

A

individual differences in cognitive processes or neural networks underlying task performance allow some people to come better with the decline in brain structures than others

22
Q

mesures of cognitive reserve

A

intelligence (crystallised intelligence)
level of education
work level
literacy
integrity of social relations
activites in spare time

23
Q

+ve and -ve influences on cognitive reserve

A

+ve
- mental stimulation
- active lifestyle
- social stimulation
- cognitive remediation

-ve
- poor education
- mood disturbance
- poor nutrition
- alcohol/drug abuse
- poor health

24
Q

low vs high cognitive reserve

A

**People with a low cognitive reserve **
- Show relatively *early a decline in cognitive performance *relative to the decline in brain structures.

People with a high cognitive reserve
- Show relatively late a decline in cognitive performance relative to the decline in brain structures

25
Q

three factors that have major influence on cognitive performance

A

Three factors that have a major influence on cognitive performance:
1. Age
2. Level of education
3. Gender

Always compare a performance with the performance of people of the same age, the same gender, and the same level of education.

26
Q

When is behaviour considered impaired?

A

Definition: a performance is considered ‘impaired’ when a person obtains a score that is > 2 SD below the average of the normal data sample.

27
Q

Gerontopsychology definition

A

is the study of stability and change in behaviour and experience during later life. Early gerontology viewed ageing as a process of decline, but modern approaches recognise multidirectional changes and stability.

shift in focus -> pathological ageins to healthy ageing focusing on resources to support wellbeing.

key idea: ageing doesn’t always lead to decline, sometumes development and stability.

28
Q

Fluid and Crystallised Intelligence

A

Fluid Intelligence:
- Abilities related to problem-solving, reasoning, and memory.
- Declines with age, especially in tasks requiring speed and working memory.

Crystallised Intelligence:
- Knowledge and skills accumulated through life, such as vocabularies.
- Remains stable or improves with age, showing multidirectional.

29
Q

Cognitive Health and Plasticity

A

Cognitive Health: refers to an individual’s ability to maintain stable cognitive performance despite environmental challenges.
Plasticity: The brain’s capacity to adapt through structural and functional changes.
- Cognitive reserve: higher education and intellectual activities build resilience against cognitive decline.
- active coping: the brain compensates for losses by reorganising networks or recruiting new pathways.
-
Example: individuals with higher educational attainment show better cognitive function despite similar levels of brain pathology.

30
Q

QoL

A

a multidimensional concept integrating subjective satisfaction and objective measures of functional capacity

31
Q

types of QoL

A

**Subjective QOL (sQOL): **
- measures through self-reports of life satisfaction and goal achievement.
- Examples: SWL (Satisfaction with Life Scale)
**Objective QOL (oQOL): **
- Assessed using external metrics like health impairments.
- May not reflect personal satisfaction or functionality.
**Functional QOL (fQOL): **
- Emphasises the perceived functionality of resources to achieve meaningful goals.
- Example: adapting to reduced physical abilities by gardening instead of farming.

32
Q

Cognitive Reserve (CR)

A

cognitive reserve (CR) refers to the brain’s ability to withstand damage or pathology without showing clinical symptoms.
- Some individual’s show no cognitive impairment despite significant Alzheimer’s disease (AD) pathology at autopsy.
- CR accounts for variability in the effects of brain pathology on cognitive function.

33
Q

core idea CR

A
  • ## CR explains how the brain uses pre-existing cognitive processes or compensatory mechanisms to resist the clinical effects of damage.
  • Distinct from brain reserve which is linked to structural factors like brain size or neuronal count.

Epidemiological Evidence:
- High education, complex occupations, intellectual activities, and active lifestyle lower dementia risk.

34
Q

cognitive reserve

Theoretical Issues CR

3 issues

A
  1. Mechanisms of Reserve:
    o The exact processes by which CR protects against pathology are unclear.
    o CR likely involves flexibility in brain networks and the use of alternative strategies for tasks.
  2. Decoupling of Structure and Function:
    o CR does not prevent brain pathology but mitigates its effects on cognitive functions like memory.
    o Brain integrity may be compromised, but cognitive function remains relatively preserved.
  3. Brain Maintenance:
    o Life exposures like mental stimulation or exercise may not only enhance cognitive reserve but also promote brain maintenance:
     Example: Reduced hippocampal atrophy in those with mentally stimulating lives.
35
Q

methods used to estimate CR

Individual Characteristics

A
  • Includes demographic and lifestyle factors like education, occupation, and intellectual engagement.
  • Easy to quantify but may oversimplify a multidimensional mechanism.
36
Q

methods used to estimate CR

Cummulative Life Experience

A
  • Considers a lifetime of experiences (academic, social, occupational, leisure).
  • Example: The “Lifetime of Experiences Questionnaire” captures these influences.
  • Limitations:
    o Summarising experiences might obscure the effects of the most significant variables.
37
Q

method used to estimate CR

Intellectual Function

A
  • Measures like vocabulary tests or reading tasks assess crystallised knowledge.
  • Advantages:
    o Reflects lifetime intellectual achievement.
  • Disadvantages:
    o Can be affected by diseases like language-dominant dementia
38
Q

methods to estimate CR

Brain Network Pattern

A
  • Functional imaging identifies brain networks linked to CR.
  • Advantages:
    o Provides a universal, culture-independent measure.
    o Useful for longitudinal studies and intervention evaluations
39
Q

application CR in Clinical practive

Diagnosis Consideration

A

o Tailor CR indicators (e.g., education, IQ) to individual patients.
o Use neuroimaging to detect pathology in high-CR individuals who appear cognitively normal

40
Q

applications of CR in clinical practice

Cognitive Decline

A

o CR delays symptoms but accelerates decline once pathology surpasses a threshold.
o Patients with high CR may show rapid decline after reaching this “point of inflection.”

41
Q

application of cognitive reserve in clinical practive

Treatment Implications

A

o High-CR individuals might benefit from early intervention, as treatment is most effective with minimal pathology.

o Lifestyle recommendations (e.g., mental stimulation) can support CR but are not proven preventative measures.

42
Q

key concepts CR

Neural Reserve and Compensation

A
  • Neural Reserve:
    o Natural variability in brain networks’ efficiency, capacity, and flexibility.
  • Neural Compensation:
    o Recruitment of alternative brain regions or networks to compensate for damage.
43
Q

key concepts CR

CR and Task-Specific Variability

A

verbal memory = multiple cognitive routes, more resitant to pathology

spatial or visual tasks = fewer compensatory strategies

  • Cognitive reserve explains why individuals with similar levels of brain pathology can exhibit vastly different cognitive outcomes

High CR ppl = resistant to clinical symptoms despite pathology, but once symptoms appear decline is rapid due to pathological burden

  • Interventions to build CR through education, mental stimulation, and active lifestyles are promising but not fully established