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W8 Flashcards

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1
Q

what are the common characteristics of LSLS?

A
  • multiple collaborators with multiple discipline
  • multiple sites
  • long designs with diff cohort
  • diverse research q, methods, databases
  • rich, enduring legacies
  • neighboring disciplines: biomedical, psych, methodology, institutional, helping and care, epidemiology
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2
Q

what is step 1 of LSLS Logic?

A

with aging come neurocognitive and other health transitions
- initially healthy older adults naturally transition into one+ general and brain-health-related trajectories leading toward clinically diagnosed conditions
- brain related transitions with age

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3
Q

what is step 2 of LSLS?

A

with longitudinal data the aging transitions can be tracked
- long-term trajectories in to and out of transition phases can be tracked for NA individuals as well as selected clinical groups

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4
Q

what is step 3 of LSLS?

A

with long-term tracking, markers, inflection points, and individual differences can be identified
- following individuals over long periods can lead to: characterization of individual differences in trajectories, detection of individual trajectory subtypes, identification of inflection points, detection of early markers of later NDD, evolution of roles of risk and protection factors

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5
Q

what is step 4 of LSLS?

A

with marker identification, progress in understanding aging conditions
-> progress toward descriptive clarity and explanatory understanding of biological, neurological, health, and cognitive precursors of transitions reflecting stability in NA, decline of MCI, onset of dementia and healthy, resilient or exceptional BA

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6
Q

what is step 5 of LSLS?

A

with progress in understanding aging conditions, precursors can be identified and interventions can be tested
- early markers indicate mechanisms of differential pathways of NDD
- explanatory knowledge, potential targets of interventions to delay neg outcomes and promote pos trajectories

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7
Q

what is step 6 of LSLS?

A
  • delaying AD can help to reduce prevalence rates (by ~50%)
  • prevalence reduction could substantially lessen familial and personal suffering, produce extensive relief and cost savings for informal care and public health)
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8
Q

what are examples of LSLS?

A
  • Berlin Aging Study
  • Betula Project
  • PATH Through Life
  • Maastricht Aging Study
  • Nun Study
  • religious Orders Study
  • Seattle Long Study
  • Victoria Long Study
  • Swedish National Study of Aging and Care
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9
Q

what was the disadvantage to the Nun study?

A
  • extrapolation of findings from this unique population may be limited
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10
Q

what was the advantage of the Nun study?

A

convent archives

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11
Q

how do the factors that confide the findings get eliminated?

A

relatively homogenous adult lifestyles and environments of women

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12
Q

why are the Nuns a good participants for AD study?

A

abstain from RF like smoking and drinking

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13
Q

what did Dr.David Snowden do?

A

studied predictors of Ad and healthy brain aging in a homogenous cohort

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14
Q

why were the Nuns aging gracefully and did not have memory loss when having AD?

A

active lifestyle and educated

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15
Q

what was a predictor of AD in the Nun study?

A

lower third in idea density were 60 times more likely to have AD-like brains post-mortem

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16
Q

compare low and high density in AD patients?

A

low were early AD
high were late onset

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17
Q

what was the mindset of the Nuns?

A

thought of participation was a service not a requirement
- thought getting her brain checked out kept her out of trouble

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18
Q

what was the most interesting part of the study?

A

the brains had lots of pathology but they weren’t demented

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19
Q

what was the difference between the Swedish and Nun study?

A

expanded from a small homogenous to a large heterogenous sample

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20
Q

what is SNAC?

A

swedish national study of aging and care
- recording of provision of care for persons over 60

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21
Q

what was the continuation of SNAC-K?

A

Kungsholmen
- clinical examination over 60 yrs
- neuroimaging long sub0study

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22
Q

what was the goal of SNAC-K?

A

understand aging process and identify possible preventative strategies to improve health and care

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23
Q

what was the model for SNAC-K?

A

conceptual model
- lifespan
- developmental approach
- rf and pf
- determinants of health outcomes
- health defined broadly

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24
Q

what were the target processes and outcomes?

A

physical: brain aging, multi- and co-morbidities, cog and physical aging
psychological: subjective health, satisfaction and well-being
social: integration and engagement

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25
Q

what are the aims of SNAC-K?

A
  • examining genetic, health, social, cog, sub, lifestyle factors that risk/protect healthy aging
  • examine rf and pf associated with NDD, multi-morbidity, diseases
  • examining natural history of NDD from pre-clinical to clinical phases, resolution
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26
Q

who created SNAC-K?

A

Dr Laura Fratiglioni

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27
Q

who participated in SNAC-K?

A

60-99
- CSL
- OO (78-99): 3 yr interval
- YO (60-78): 6 yr

28
Q

what does SNAC-K study?

A

nurse interview: demographic background, substance use, physical fxn, health practices
clinical form
cognitive functioning
background/other

29
Q

what were the social and public health results from SNAC-K?

A
  • ad public health crisis: increase disorders with aging (MCI and dementia)
  • quality of drug use (prescription errors and meds misuse)
  • economic: model costs over time

-> greater avg severity over time
-> lower and diminishing prevalence and decreasing overall costs

30
Q

what were the vascular rf and dementia results?

A

rf and diseases: smoking, alcohol, heart conditions, mild stroke, diabetes
- increased risk of dementia

31
Q

what is the correlation to diabetes and MCI?

A

increased risk
accelerated rate of progression

32
Q

why do some with APOE e4 not have dementia?

A

it is a risk but not a determinant
- not all carriers convert

33
Q

who has the greatest to the least risk of AD?

A

e4-e4
e4-e3
e3-e3

34
Q

what is risk reduction for APOE e4?

A

risk of dementia for e4 carriers was reduced when they had at baseline - low vascular RFs, higher education, more leisure activities

35
Q

what are the results of lifestyle moderates diabetes-dementia risk?

A

leisure activity engagement and rich social network may compensate (reduce risk associated with diabetes)
- 48% of diabetes dementia could be prevented with active social-leisure lifestyles

36
Q

what are the results of environmental pollution and cog health?

A

long-term exposure is an RF
- CVD most affected
- rf for depression in older adults
- transportation noise also a dementia for RF

37
Q

what did the VLS track?

A

normal aging: NA, BCA, asympt, non-demented
exceptional/resilient: healthy brain/cog aging (EBCA)
pre-clinical: transitions or classifications (SCI, MCI)
clinical status: diagnosed (AD, ADRD)
predictors and moderators: multiple rfs, pfs, biomarkers, genetics, sex/gender, exposures

38
Q

where does funding for VLS come from?

A

NIH and other

39
Q

what is the 3-point rationale?

A
  • target initially healthy cohorts: recruit successive cohorts of relatively healthy adults
  • have patience for patients: follow cohort longitudinally as they develop various aging-related conditions
  • archives are assets: maintain precise long-term archives and conduct research on patterns, profiles, predictors, rfs, moderators of cognitive changes associated with epidemiological interests in BCA and D
40
Q

what are the 3 cohorts for VLS?

A

MA-YO (55-64)
MO (65-74)
OO (75-85)

41
Q

what are the intervals between waves?

A

3-4 yr intervals b/w waves

42
Q

was this a full LONG design?

A

no
- sequence longitudinal design across 3 gens

43
Q

what are the 3 recent and integrative initiatives?

A

mci/dementia initiatives
biomarker and risk
healthy ba

44
Q

what occurred to each wave every 4 years?

A

attrition
- wave 1: mobility
- wave 2: impairment
- wave 3: morbidity

45
Q

what are the 4 clusters of cognitive health/decline indicators?

A
  • components of neurocognitive performance, change and status
  • health, disease, meds
  • biomarkers, fitness, genetics, bioage
  • background, life history, affect, activities, exposures, experiences
46
Q

what is episodic memory and why is it important?

A
  • explicit recall of personally experienced single episodes or events
  • common complaint
  • “AD warning sign”
  • early sign of NDD
  • YA > MA > YO > OO
  • gradual aging decline YO ~ MA > or equal to OO
47
Q

what is preserved in asymptomatic aging?

A

semantic memory
- memory for facts, concepts, culturally provided info, accumulated and shared knowledge

48
Q

what are the 7 steps for LSLS?

A
  • linking and extending traditional approaches (1-4)
  • tracking: descriptive forms of change (5-6)
  • memory in healthy brain and cog aging (7+)
  • exploring mechanisms and modifiers of change
49
Q

who had better episodic memory and semantic?

A

YA
OA

50
Q

what were the results for MA and EA for episodic memory?

A

same bc hard to gather data from the group

51
Q

steps 1-4 what do you learn from the data?

A
  • within-aging age differences: evident and sustained heterogeneity
  • across waves are modest and gradual group-level changes
  • disconnect b/w regularity of CSL group mean differences and actual change patterns and substantial variability in LONG trajectories
52
Q

what is the purpose of spaghetti plots?

A

exploring functional forms of memory changes
- growth curves summarize overall change across full age band

53
Q

how are spaghetti plots improved?

A

new tech in trajectory research
data-driven analytics

54
Q

what is machine learning technology?

A

unsupervised discovery of properties and patterns in big or complex data
- use data driven modeling: identify subtype patterns of trajectory distributions, determine precision predictors of each cluster, explore efficacy as AD prevention targets

55
Q

what is data-driven analystics?

A
  • secondary phenotype classification
  • differentiate between high and low risk
  • test and compare multiple predictors from risk modalities
  • mechanisms vay
  • interventions require precision
  • study stratified subgroups
56
Q

what were the results of biomarker predictors by subclass and age?

A
  • predictor patterns were diff for SMA and DMA
  • predictors were diff for YO and OO
  • sex predicted SMA, not DMA
  • age predicted DMA for YO adults only
57
Q

what is memory resilience?

A

sustained memory performance over time despite objective adversity (in addition to age) of AD genetic risk

58
Q

what is the first definition?

A

objective operational definition (APOE)
- resilient = observed when persons with AD genetic risk show memory trajectories with relatively high intercept and sustained/high slope

59
Q

what is the second for memory resilience?

A
  • focus on modifiable rf predictors of resilience
  • 22
    5 risk domains: demographic, functional, health, gait/mobility, lifestyle
60
Q

what is the third approach for memory resilience?

A

sex
gender

61
Q

what are memory resilience to AD genetic risk predictors for women?

A
  • lower pulse pressure, higher peak expiratory flow
  • faster walking and turning time
  • more social visits and volunteering
  • living with someone and being married
62
Q

what are memory resilience to AD genetic risk predictors for male?

A

fewer depressive symptoms

63
Q

what are are memory resilience to AD genetic risk predictors for both?

A

younger age
education
stronger grip
everday novel cognitive activity
less alcohol

64
Q

what occurred after W6 for later diagnosed ad?

A

word steeply declines (episodic)

65
Q

what can identifying key clusters of change patterns and testing potential decision predictors lead to?

A

progress in early detection of mci and ad risk
early detection of hbca potential

66
Q
A

Psych 403 (10 decks)

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