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Psych 403 > W10 > Flashcards

W10 Flashcards

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1
Q

from landmark 1 what are the 2 goals about caregiving?

A
  • advocate for individuals, families, care partners, and service providers. most who are developing dementia are not alone, the people contributing need support and resources
  • push for change. more action, CHANGE to care system. rid of stigma and discrimination and stereotypes. solutions for the challenges
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2
Q

what are the 2 key gaps from Landmark 1

A
  • home care and long-term care systems under strain and facing multiple crises, need to remodel dementia care
  • care partners report positive aspects of providing care, they also have challenges (money, burnout, depression, isolation)
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3
Q

what happens to the caregivers population as the dementia cases increase?q

A

they also increase

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4
Q

who are typical care partners and what is the special gen called?

A

family 58%
spouses 32%
other 10%
- sandwich or squeezed generation

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5
Q

how many hours a week are for caregiving?

A

26

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6
Q

what do caregivers do?

A

everyday activity help
medical support
psychological help
companionship
advocacy

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7
Q

what are the 4 types of support given by care partners?

A
  • assistance with daily core activities
  • assistance with self-care
  • manage support and home care
  • support changes in mood, personality and behavior
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8
Q

what are the downsides to informal partner support?

A
  • stress
    -> levels change depending on type, volume, duration, complications of care
    -> almost half of care partners show distress
  • factors changing partners stress levels
    -> own health, impairments, affecting various relationships
  • costly cycle: 7.3B for informal
  • gender: 54% of givers are W
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9
Q

what can Alz Societies do?

A
  • reduce stigma and raise public awareness
  • grow supports and services to fill gaps in healthcare
  • continue building relationships and resources for diverse communities - more stigma
  • engage people living with dementia and care partners: CCNA
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10
Q

what can health-care systems do?

A
  • provide education on risk reduction approaches to dementia
  • provide dementia education and training to broader circle of allied health prof
  • grow capacity for dementia-specialized community clinics, community and home care and long-term care
  • recognize specific needs and supports of care partners and people with D
  • provide effective support for dementia care partners through primary care and health prof
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11
Q

what can the federal gov’t do?

A
  • increase investments in research to reach goal set in NDS
  • actively work to reduce stigma against D through national awareness campaigns
  • support implementation of care partner leave more widely
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12
Q

what can provincial and territorial gov’t do?

A
  • create new community care and long-term care spaces that are D friendly
  • plan for increases in spending for homecare, social supports and long-term care
  • create policies and processes that support culturally safe dementia care
  • destigmatize and enhance supports for younger care partners
  • respond to care partner challenges
  • support workplaces in providing flexible supports for care partners
  • build up system of interventions designed to assist care partners
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13
Q

what can municipal gov’t do?

A
  • support community cultural organizations in delivering brain health programs
  • fund local support networks
  • encourage more dementia-friendly spaces
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14
Q

what can researchers do?

A
  • in ppl with D and care partners in research
  • study PF, RF and interventions over life course
  • ensure D research pop reflecr diversity in Canadian pop
  • work to develop new insights on care needs of people living with D
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15
Q

what can I do?

A

support care partners

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16
Q

what are the 3 CCNA teams that address caregiving?

A

15: issues in D care for rural populations
19: Integrating dementia patient care into healthcare sys
18: Issues in D care for Indigenous

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17
Q

what is the continuing theme?

A

integrating global and diversity considerations in research on neurogenerative diseases

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18
Q

what is the WHO pov for indigenous aging and dementia?

A

stigma, racism and racial disrimination
-> increases exposure and vulnerability to RF and reduces access to quality health services
-> experience poorer health outcomes

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19
Q

what is I-CAARE?

A

Indigenous Cognition and Aging Awareness Research Exchange

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20
Q

what is the goal and wellness intervention of I-CAARE?

A
  • break the cycle of Indigenous-specific social and structural determinents of health
  • confirmation of knowledge, wellness practices, cultural safety, equitable access and reduction of discrimination
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21
Q

what to the # look like for 2050?

A

canadian percentage decreases (3)
asian increases (2)
european decreases (1)

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22
Q

what is intersectionality?

A

multiple and simultaneous characteristics intersect to form individual’s identity in broader sys of power that can result in oppression and privilege

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23
Q

what did the genetics study indicate?

A

cognitive fxn is heritable with genetics factors contributing significantly to individual differences
- cog decline with age caries
- GWAS: genetic variants linked to cog performance and aging
- genes interact with lifestyle factors
- advances in polygenic risk scoring allow to predict cognitive abilities and risk of cog decline

24
Q

what is GWAS?

A

examine of many genetic variants discover which are associated with target phenotype and at what relative magnitude
- targets a clinicial phenotype: compares AD with normal control group

25
Q

what is a genotype?

A

identity of two alleles at specific genetic locua

26
Q

what is SNP?

A

single nucleotide polymorphisms - variation at a single position in DNA sequence
- two alleles that reflect genotype of interest

27
Q

what is a phenotype?

A

observable characteristic of genotype

28
Q

what is a primary phenotype?

A

reliably and differentiated diagnosed disease
- AD, PD, VaD

29
Q

what is secondary phenotype?

A

detectable and validated condition representing elevated risk for passage to diagnosable disease
-> clinically or empirically “classified” conditions

30
Q

how is APOE unusual?

A

3 alleles produce 3 homozygote and 3 heterozygotes variants
- 6 APOE genotypes
40% of E4 have a risk

31
Q

what is the description of a candidate gene study?

A

function of gene is tested for its implication for particular phenotype
- GWAS-identified gene: used in prediction studies of differential status, level, change, implications for bio mechanisms

32
Q

what increases the probability of an associated phenotype?

A

interaction of genetic effects such as 2 key RF or PF

33
Q

gene x gene

A

2+ “hits” or R and 2+ “doses” of P

34
Q

what are the other combos possible?

A

gene x enviro
gene x lifestyle
gene x health activity
gene x health condition

35
Q

what is polygenic risk index?

A

multiple candidate genes can be combined in risk effects to provide prediction of primary or secondary phenotype
- global or mechanism-specific

36
Q

what does environment do to the risk?

A

non-genetic influence on genetic expression and phenotype of interest
- health condition
- exposure
- exposome
- heritable

37
Q

what is the rare form of AD and what is the cause?

A

familial AD - fAD or EOAD
- PSEN1
- PSEN2
APP
- mutation causes abnormal APP leading to accelerated beta-amyloid deposition on brain
- autosomal dominant

38
Q

what is the more common form of AD?

A

sporadic AD - sAD or LOAD
- variety of RF
- GWAS
- most prominent genetic rf is APOE e4 - 40%

39
Q

which type of AD manifests earlier?

A

fAD

40
Q

what are the 3 approaches to genotypes as biomarkers of AD?

A

GWAS: coverage, large samples, discovery, prediction
candidate gene studies: APOE major predictor and moderator, other RF less consistent
genetic interactions: search for intensification or magnification or moderation of genetic risk on AD. AD polygenic risk indexes, enhanced prediction of early preclinical change and transitions and AD conversion

41
Q

what did GWAS and AD study find?

A

unbiased approach to identifying regions of genetic association with trait or disease
- quantitatively sift through genes to identify “hits” with target disease

42
Q

what is the GWAS “Manhattan Plot”

A

scatter plot showing SNPs along x-axes and statistical significance along y-axis after adjusting for age and sex

43
Q

what are the traits for genetics of aging and cognition?

A
  • genetic and heritable
  • domain-specific or process-focused
  • differentially changing
  • cognitive or clinical diagnosed status
  • multiple approaches
44
Q

what is APOE?

A

most prevalent brain lipoprotein expressed in 3 isoforms
- deposited in neurotic plaques and tangles
- e4/e4 = 50% chance of AD
- can impair plasticity, hipp atrophy, glucose metabolism, brain inflammation, cerebrovasculature

45
Q

what is the most prevalent genetic indicator of sporadic AD?

A

apoe e4

46
Q

what percentage were identified with APOE e4?

A

60%

47
Q

who has the reduced risk of AD later in life?

A

apoe e2 carriers

48
Q

what is the incident MCI with e4 carriers?

A

58% compared to 22% having stable NA with e4

49
Q

what were the results form the Lothian Birth Cohort?

A

differences in e4-related cognition at age 11 exacerbated by age 79
- from 70-80 narrow e4-related memory gaps widen

50
Q

what are the other biomarkers used to mark ad?

A

AB and tau

51
Q

what are the stages to convert apoe in therapy?

A
  • convert apoe e4 to e3 -> increase lipidation -> ab decoy peptide -> anti-apoe e4 mAbs -> APOE mimetic peptide -> gene transfer to apoe e2
52
Q

what is the effect of E4 on episodic memory learning in NA?

A

e4-e4: learning declined faster around 75 compared to no e4 which was 90 (better performance)

53
Q

can there be resilience to e4 adversity?

A

yes

54
Q

what are the results from genetics x health?

A

no independent effects of APOE on EM or SM
PP negatively affects EM, not SM -> better PP, better memory, worse PP
APOE x PP interaction -> APOE moderates PP effects on EM

55
Q

what is the effect on VH?

A

men have a steeper decline than females but F still decline just not as steep

56
Q

what is the difference between M and F with e2 carriers?

A

f still have good memory with good vh
m have poor memory with good vh

57
Q
A

Psych 403 (10 decks)

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