W10 Flashcards
from landmark 1 what are the 2 goals about caregiving?
- 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
what are the 2 key gaps from Landmark 1
- 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)
what happens to the caregivers population as the dementia cases increase?q
they also increase
who are typical care partners and what is the special gen called?
family 58%
spouses 32%
other 10%
- sandwich or squeezed generation
how many hours a week are for caregiving?
26
what do caregivers do?
everyday activity help
medical support
psychological help
companionship
advocacy
what are the 4 types of support given by care partners?
- assistance with daily core activities
- assistance with self-care
- manage support and home care
- support changes in mood, personality and behavior
what are the downsides to informal partner support?
- 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
what can Alz Societies do?
- 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
what can health-care systems do?
- 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
what can the federal gov’t do?
- 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
what can provincial and territorial gov’t do?
- 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
what can municipal gov’t do?
- support community cultural organizations in delivering brain health programs
- fund local support networks
- encourage more dementia-friendly spaces
what can researchers do?
- 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
what can I do?
support care partners
what are the 3 CCNA teams that address caregiving?
15: issues in D care for rural populations
19: Integrating dementia patient care into healthcare sys
18: Issues in D care for Indigenous
what is the continuing theme?
integrating global and diversity considerations in research on neurogenerative diseases
what is the WHO pov for indigenous aging and dementia?
stigma, racism and racial disrimination
-> increases exposure and vulnerability to RF and reduces access to quality health services
-> experience poorer health outcomes
what is I-CAARE?
Indigenous Cognition and Aging Awareness Research Exchange
what is the goal and wellness intervention of I-CAARE?
- 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
what to the # look like for 2050?
canadian percentage decreases (3)
asian increases (2)
european decreases (1)
what is intersectionality?
multiple and simultaneous characteristics intersect to form individual’s identity in broader sys of power that can result in oppression and privilege
what did the genetics study indicate?
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
what is GWAS?
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
what is a genotype?
identity of two alleles at specific genetic locua
what is SNP?
single nucleotide polymorphisms - variation at a single position in DNA sequence
- two alleles that reflect genotype of interest
what is a phenotype?
observable characteristic of genotype
what is a primary phenotype?
reliably and differentiated diagnosed disease
- AD, PD, VaD
what is secondary phenotype?
detectable and validated condition representing elevated risk for passage to diagnosable disease
-> clinically or empirically “classified” conditions
how is APOE unusual?
3 alleles produce 3 homozygote and 3 heterozygotes variants
- 6 APOE genotypes
40% of E4 have a risk
what is the description of a candidate gene study?
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
what increases the probability of an associated phenotype?
interaction of genetic effects such as 2 key RF or PF
gene x gene
2+ “hits” or R and 2+ “doses” of P
what are the other combos possible?
gene x enviro
gene x lifestyle
gene x health activity
gene x health condition
what is polygenic risk index?
multiple candidate genes can be combined in risk effects to provide prediction of primary or secondary phenotype
- global or mechanism-specific
what does environment do to the risk?
non-genetic influence on genetic expression and phenotype of interest
- health condition
- exposure
- exposome
- heritable
what is the rare form of AD and what is the cause?
familial AD - fAD or EOAD
- PSEN1
- PSEN2
APP
- mutation causes abnormal APP leading to accelerated beta-amyloid deposition on brain
- autosomal dominant
what is the more common form of AD?
sporadic AD - sAD or LOAD
- variety of RF
- GWAS
- most prominent genetic rf is APOE e4 - 40%
which type of AD manifests earlier?
fAD
what are the 3 approaches to genotypes as biomarkers of AD?
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
what did GWAS and AD study find?
unbiased approach to identifying regions of genetic association with trait or disease
- quantitatively sift through genes to identify “hits” with target disease
what is the GWAS “Manhattan Plot”
scatter plot showing SNPs along x-axes and statistical significance along y-axis after adjusting for age and sex
what are the traits for genetics of aging and cognition?
- genetic and heritable
- domain-specific or process-focused
- differentially changing
- cognitive or clinical diagnosed status
- multiple approaches
what is APOE?
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
what is the most prevalent genetic indicator of sporadic AD?
apoe e4
what percentage were identified with APOE e4?
60%
who has the reduced risk of AD later in life?
apoe e2 carriers
what is the incident MCI with e4 carriers?
58% compared to 22% having stable NA with e4
what were the results form the Lothian Birth Cohort?
differences in e4-related cognition at age 11 exacerbated by age 79
- from 70-80 narrow e4-related memory gaps widen
what are the other biomarkers used to mark ad?
AB and tau
what are the stages to convert apoe in therapy?
- convert apoe e4 to e3 -> increase lipidation -> ab decoy peptide -> anti-apoe e4 mAbs -> APOE mimetic peptide -> gene transfer to apoe e2
what is the effect of E4 on episodic memory learning in NA?
e4-e4: learning declined faster around 75 compared to no e4 which was 90 (better performance)
can there be resilience to e4 adversity?
yes
what are the results from genetics x health?
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
what is the effect on VH?
men have a steeper decline than females but F still decline just not as steep
what is the difference between M and F with e2 carriers?
f still have good memory with good vh
m have poor memory with good vh
