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W3 Flashcards

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1
Q

what is the key goal of research design in aging, ND, and dementia?

A

provide both general-group and person-centered info about long-term aging pathways leading toward relatively healthier brain aging or sustained typical brain aging or towards CI and dementia

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2
Q

what is the key focus of research in aging and AD?

A

designing, collecting, analyzing and interpreting data
- reflect and display common patterns and diverse heterogeneities of individual and group cog and brain health aging

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3
Q

what is the key research interest of research?

A

identifying individual and group differences and changes in transitions, directions, RF, predictors (biomarkers) and responses (RR)

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4
Q

what are the interests associated with “change”?

A

description of change: what, when, how
explanation of change: why
differential change: degree of dynamic heterogeneity
modifiability of change: can we change the direction of change?

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5
Q

what is the fundamental feature of research design?

A

time -> change occurs over time
- explicit research attention to framing, studying, displaying or approx relevant aspects of group or individual differences may change over time

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6
Q

what do research designs require?

A

time-structured design and change-sensitive measures

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7
Q

what is the goal of research design?

A

detect and measure direction, rate, variability, responsivity

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8
Q

what are the two basic types of research design?

A

cross-sectional design
longitudinal design

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9
Q

what is CSL?

A

comparing diff groups on one occasion of measurement

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10
Q

what is LONG design?

A

following all individuals in one or more group across more than one time point or across clinical status transitions
(NA->MCI)

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11
Q

what are the strengths and weaknesses of CSL?

A

S: quick and inexpensive
W: detects group or age diff only, historical cohort effects

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12
Q

what are the strength and weaknesses of LONG?

A

S: age changes and transitions detectable
W: time consuming, expensive, historical cohort effects

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13
Q

what is the historical cohort effect?

A

aggregate of individuals who experiences same aging-related risk or protection exposures
- same historical time interval and as similar dosages of experience
- “Birth Cohort”

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14
Q

is historical and clinical cohort the same?

A

no
- clinical refers to groups of individuals classified according to objective clinical characteristics

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15
Q

what is the long-term effect of historical cohort effect?

A

persons may develop differently depending on cohort membership

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16
Q

what creates cohort differences?

A

major historical events or trends

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17
Q

on a graph how do you differentiate CSL from longitudinal?

A

CSL has no connecting points and LONG has connecting points

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18
Q

what is the limitation for CSL?

A

no direct info on intraindividual change and variability, or individual differences in change

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19
Q

what is the limitation for LONG?

A

direct indication of age changes but no necessarily the same profile across individuals, successive cohorts, diff generations

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20
Q

what is a limitation for both designs?

A

descriptive - no mechanisms or predictors

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21
Q

what is the complexity for inter-individuals differences?

A

no single normative path

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22
Q

what is the complexity for intra-individual variability?

A

within domain individuals can vary

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23
Q

what is the purpose of a theoretical model?

A

representation or framework for how things might work and how they might be explored
- roadmap

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24
Q

what are the methods for eval models?

A

usefulness in representing research results and providing direction for productive and theoretically important new studies and results

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25
Q

what do modern models do?

A

attempt to represent dynamic and interactive complexities of transitions in brain and cog aging

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26
Q

what are the 2 models of NA-MCI-AD transitions?

A

linear vs dynamic polygon

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27
Q

compare original dynamic polygon model vs recent models

A

og: broad integrative with important implications (dynamics and potential)
recent: suggest future steps, even broader view, dynamic interactions, broader health biomarkers

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28
Q

what are some applications for the polygon model?

A

early detection
intervention

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29
Q

what do the new models of AD pathways imply?

A
  • time structured: dynamic, long-term
  • interactive: expected, tested, within/across RF and biomarker domains
  • modifiable and non-modifiable distinction
  • multiple outcomes: CN, CI, CND
  • intervention targets
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30
Q

what is the CCNA?

A

Canadian Consortium on Neurodegeneration in Aging
- 2020 Roadmap for ADRD research

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31
Q

what are the 2 types of large-scale epidemiological studies?

A

cross-sectional sequential design
long sequential design

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32
Q

what are the advantages of doing Long sequential designs?

A
  • acceleration: “band” of aging covered can expand rapidly
  • epidemiological progress: range of biomarkers, multiple modalities of predictors and mechanisms of actual change and outcomes can be tested
  • early detection
  • transition tracking
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33
Q

what is the disadvantage of doing Long sequential design?

A

v expensive and time consuming

34
Q

what is considered to be observational research?

A

CSL
LONG
LONG-SEQ
BIG DATA

35
Q

what is considered to be intervention research?

A

experience
training
therapeutic

36
Q

what is a “gold standard” intervention?

A

RCT
- precise design features for supporting intervention efficacy

37
Q

what is RCT?

A

specialized experiment for determining efficacy of observationally indicated and theoretically supported intervention for treating, curing or delaying adverse condition

38
Q

what is the key feature of RCT?

A

random allocation to specific treatment or placebo

39
Q

why do randomization?

A

eliminate bias or selection effects and help mask/blinding treatments

40
Q

what are the requirements for RCT to occur?

A

-registered to world-wide clinical trials data base
- go on record with protocol paper
- document and follow procedural rules

41
Q

what are the 2 new identifiable phases between NA and AD?

A

SCD
MCI

42
Q

what is SCD?

A

subjective cognitive decline
- self-reported awareness

43
Q

what is the challenges of SCD?

A

measurement
veridicality
predictive

44
Q

what is SMD?

A

subset of SCD

45
Q

what is MCI?

A

mild cog impairment
- awareness plus objective evidence and clinical judgement regarding multiple factors

46
Q

is MCI a disease?

A

no it is a classification not a diagnosis

47
Q

what are the issues with MCI emergence?

A

can later segment of PreAD be differentiated, classified, validated and clinically useful?

48
Q

what is the goal of MCI research?

A

seeking earlier identifiable phases for reliable signals of impending ad

49
Q

how to verify MCI?

A

evidence for reliability (repeat) and validity (success of predication)

50
Q

how is MCI research useful?

A

organize understanding of early AD risk, operationalizing preclinical period, providing valid target group for intervention

51
Q

who was important for MCI research?

A

ronald petersen

52
Q

what was Petersen’s goal?

A

develop models for predicting dementia from cog impairment signs in otherwise NA

53
Q

what did Petersen question?

A

the boundary zones between NA and AD

54
Q

what was the review in 2000?

A

MCI emerging as preferred term to define cog impairment that may be prodrome to AD

55
Q

what was Petersen’s role and goals?

A
  • developer and early leader in MCI
  • identify transitions between NA to MCI and then predict transitions from MCI to AD
56
Q

what was Petersen’s approach?

A

5 + 1
- memory complaint
- objective memory impairment
- intact general cognition
- preserved activities of daily living
- not demented
** clinical judgement may be involved in final classification of an individual

57
Q

what was the MCI status report?

A
  • lots of research
  • assessment progress in testing clinical prediction validity
  • clinical differentiation -> more than one MCI for AD and ADRD
58
Q

what is amnestic MCI?

A

memory-specific MCI most closely related to AD and outcome

59
Q

what are the challenges for MCI?

A
  • MCI status should predict AD better than NA and SCD groups
  • improve classification precision -> reduce uncertainty
  • dilemma in NA-MCI-AD transitions
60
Q

what was the contingent conclusion?

A

MCI is heterogenous classification
-> growing evidence of diversity in MCI: clinical presentation, NDD-related subtypes, pathways to and from MCI

61
Q

what are the 3 challenges associated with heterogeneity in MCI?

A
  • how to optimally weight various clinical-cog criteria for more precise MCI classification
  • how to eval and account for diversity
  • how to consider and integrate objective info, sub reports, informant reports, skilled clinical judgement
62
Q

what is MCI and what is MCI not?

A

MCI is not a clinical destination or aging end-state
- not a disease state or diagnosis

MCI is a transition phase with heterogeneity and multi-directionality
- more objective than SCD or pre-clinical
- less objective and certain than AD
- probabilistic but represented elevated risk for AD

63
Q

what kind of research design is recommended for MCI?

A

LONG

64
Q

what are some assessment and measurements for MCI?

A
  • cognitive domains (memory, global impair, processing speed)
  • biomarkers and RF
  • multi doses and interactions
65
Q

who discovered MCI “reversion”?

A

Katie Palmer and Backman

66
Q

what was the MCI reversion project called?

A

Kungsholmen project

67
Q

what was the Kungsholmen project?

A

13 yr LONG pop-based study of aging and dementia
plus 75 age sample
age-related risk for MCI and AD

68
Q

what did Palmer discover?

A

prevalence of 15% of baseline non-demented participants
heterogenous development
MCI 3x more likely to progress to dementia than 85% healthy older adults

69
Q

what are the characteristics of MCI reversion?

A
  • reversion of SCD -> pre-MCI-classification with differential trajectories and unclear prospects
  • SCD has fluid boundaries and variable change patterns
70
Q

why can MCI reverse?

A

more heterogenous than AD
complex process that reflects individualized changes
not a final outcome

71
Q

what was the goal of the reversion study?

A

discover characteristics of individuals with MCI who revert to NA status and what happens next

72
Q

how many reverted, continued, converted?

A

16
64
20

73
Q

what predicts reversion?

A

MMSE
clinical dementia rating scale
functional activities
APOE status

74
Q

what happens post-reversion?

A

MCI-NA reverters greater risk for later cog decline

75
Q

what was the first consensus about MCI?

A

phase of AD when experiencing gradually progressive cog decline that results from accumulation of AD pathology in brain

76
Q

what was the second consensus about MCI?

A

amnestic and non-amn cognition should be tested objectively
- LONG cognitive change essential or subjectivelu through informants
- eval biomarkers and RD

77
Q

what did Brainerd explore?

A

APOE and MCI
- relatively reliable predictor of MCI

78
Q

what did Jack explore?

A

preclinical MCI with cascade theories of AD development
- cascade leading from MCI and AD and progressing to AD could be apparent in MCI and accelerated or delayed by AD RF
- moderator: stratification by APOE e4
- risk predictors: amyloid deposition, neuronal injury, neuroimaging evidence

79
Q

what can large LONG studies do?

A
  • examine genetic, ad biomarker, vascular risk MCI factors
  • predict status, emergence, reversion and stability
  • follow and test transitions and trajectories
80
Q

what does APOE e4 do?

A

intensified the effect of other AD risk factors on MCI emergence

Psych 403 (10 decks)

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