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Growth and Development > cognitive function > Flashcards

cognitive function Flashcards

1
Q

cognitive function

A

info processing involves
- memory
- attention
- perception
- planning actions
- problem solving
- visuo spatial activties
- mental imagery

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2
Q

biological theories

A

variations in cognitive ageing - different theories to why
physiological/molecular- damage free radicals to vital molecules (collagen, dna, protein- oxidative stress) and or accumalation toxic waste cell products
genomic- somatic mutations, genetic errors or self programmes cell death (apoptosis)

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3
Q

rate of ageing in different systems

A

female fertility- large drop after 35 to stop at around age 50
different in men and women due to drop in female fertility - hormones involved in lots of processes in body

order from slowest to faster
- nerve conducting velocity
- maximum heart rate
- kidney blood flow
- max breathing capacity
- max work rate (o2 uptake)

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4
Q

system changes in ageing

A

in disease free organs there is not much age related loss
cardiac- eg HR shows no significant change-physical exercise capacity- slight decrease
pulmonary- eg total lung capacity shows no sig change but vo2 max decreases
renal- renal blood flow decreases and glomerular filtration rate decreases
can maintain the function of these organs/systems through diet and exercise

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5
Q

how body affects brain function

A

vascular function (heart attacks and athersclerosis) and lung function (hypoxia= lack of o2 to brain)
deficits sensory system- cataract, glaucoma, deaf
immune stess and endocrine system by hormomes
kidney- liver function and metabolism- diabetes
all can affect functioning of brain

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6
Q

testing brain function

A

verbal meaning test cross sectional vs longitudinal
longitudinal scores increased with age
cross sectional scores decreased a lot with age

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7
Q

cohort effects

A

different groups of people havr been exposed to different things in their life
lack of antibiotics- living through war throughout life for older individulas mean they are stronger now so may age beteer than we will now
longitudinal stiduies show long periods of stability followed by decline but decline is greater on some cogntive tasks compared to others

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8
Q

stroop test

A

read colour font not colour name
lots of frontal lobe is active
older people are a lot slower

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9
Q

normal ageing

A

age related decline is particularly apparent on more complex (speeded) tests
complex dual tasks- test requiring inhibition of distracting info or inhibitiom of over learned responses

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10
Q

oxidative stress and ageing

A

dopamine plays a role in info processing
amphetamines (dopamine) improve WMM and speed but haldol impairs this
D1,2 receptor binding decreases with age but is also related to deficits in cognitive and motor functioning
response has inverted U shape
dopamine synthesis stimulates free radical levels

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11
Q

free radical damage and hypoxia

A

ageing- damage related changes
- protein aggregation/misfolding, structural modification, loss of resistance to oxidative stress
- failure to repair damages
- hypoxia- lack of o2 to heart, lungs and vessel
- 4x risk of dementia after stroke = lack of o2 to parts of brain

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12
Q

glutamine toxicity

A

GLUT- major excitatory amino acid
hypoxia- GLUT increases- toxic at higher levels fro neurones
plays a role in age related cognitive decline- huntigtons disease and alzheirmers- memantine affects GLUT NDMA receptors

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13
Q

pathological brain ageing

A

alois alzheimer- studies 51 year old women with progressive cogntiive impairment, hallucinations, delusions, psychosocial incomptence
misfolding of protein- in pyramidal cell occupied by neurofibrillary tangle
found diffuse amyloid plaque where cell can no longer function

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14
Q

dementia

A

types
- alzheimers
- vascualr dementia
- frontemporal dementia
- lewy bodies dementia- linked to parkinsons - vivid hallucinations + language issues

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15
Q

alzheimers

p

A

post mortem signs
- extracellular amyloid
- intraneuronal neurofibrally tangles (NFTs)
- neuron death
- synaptic loss

alzheimers can be confirmed post morterm by semi quantitative method counting neuritic plaques
prevention methods need to start very early on

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16
Q

AZ- clinical manifestation

A

early loss of short term memory (recall and learning), day to day forgetfulness
progressive, gradual loss of longer term memory
other cognitive impairments- visuo spatial and temporal orientation, language, planning, personality change- visual sensitivity may occur early on
will impact social/occupational functio and are not caused by another morbidity

17
Q

vascular dementia

A

multiple infarcts in corticol/sub corticol grey matter or white matter demylination- lacunae, incomplete infarction, loss of myelin sheet
associated with atherscelorsis, hypertension and usual heart disease risk factors
dont see lack of memory in first place but tends to progress later on
lacunae implants caused by lack of o2 ot brain

18
Q

clinical differences in VaD and AD

A

verbal memory is often spared in VaD while executive function is bettwe in AD
- criteria that require verbal memory to be impaired have low specificity
- lots ofoverlap between dementia categories ]
- need other info including history anf physical examination and lab measures

19
Q

diagnosis

A

memory test- HVLT, CVLT
tests for global cogntiive function- MMSE (mini mental state examination)
other cognitive tests- BNT, CLOX, PAL

20
Q

verbal learning test

A

individuals with dementia struggle to cluster words and see similarities between the words which makes it harder for them to remember a large amount of words

21
Q

risk for alzheimers disease

A

what is good for the heart is good for brain
different risk factors and different diseases leading to dementia

22
Q

dementia prevention

A

primary- over the lifespain to prevent pathology
secondary- in prodomal phase- mild cognitive impairemet to prevent dementia onset
tertiary- once people have dementia to reduce rate worsening of symptoms

23
Q

genetic risk factors

A

APOE- E4 allele
having this genotype is associated with a greater risk but 20% of people who do not get dementia carry this genetic risk factors + 40% of people with alzheimers do not carry it

24
Q

dementia prevalence

A

sex differences
female- loss of sex steorids that support brain function
for women- dementia is number 1 driver of mortality
higher in women may be because females live for longer which means there is more time for thwm ro develop it

25
Q

dementia and education

A

good education is important to create congitive reserve
low education a sig risk for AD
low SES at 20 yrs age associated with increased risk (even if SES increases later in in life)
suggests early life factors

26
Q

childhood IQ§

A

relationship between education and dementia reflects relationship between childhood IQ and dementia
childhood (paternal/maternal) experience- safe environment- toxicity, nutrition, stimulating environment
brain reserve capacity= amount pathology needs to override initial reserve

27
Q

risk factors

A

often occur together and are modified by demographics
changes in risk factors occur over lifetime
high blood pressure 15 years before onset but decrease in BP 1-2 yrs before onset of dementia
people forgte to eat + lose body mass, cholesterol + BP goes down

28
Q

micronutrients and cognition

A

antioxidant vitamins- E,C,A- may protect against cognitive decline
vitamin E in nits, seeds + leafy greens

29
Q

anemia

A

fatigue, breathlessness, memory ussues
lack of o2 supply due to lack of RBCs
causes- iron deficiency

30
Q

vit b12

A

meat, fish, dairy and eggs
deficient - pale yellow skin, red swollen tongue, PNS- pins and needles

31
Q

folate

A

vit b9 in leafy greens and oranges
homocysteine- harmul amino acid broken down by b12 and folate but can be very damaging if it is not broken down- associated with heart disease and dementia
low folate or low vit b12 levels associated with an increased risk of dementia and AD

32
Q

homocysteine

A
  • leads to atherosclerosis, ischaemia
  • activates NMDA receptor
  • DNA hypomethylation- oxidative stress
  • Activates cell cycle, leading to tangles and apoptosis
  • Sensitives neurons to excitotoxins and beta amyloid toxicity and is associated with rate of MTL atrophy
33
Q

b vitamins and cog dysfuntion

A
  • B vitamins help to reduce brain atrophy by 30% in those with memory problems but not dementia
34
Q

folate/folic acid

A
  • Folate is natural form found in foods- bioavailabity is 50-70%- natural folates in food are progressively inactivates
  • Folic acid is found in supplements + converted in the body to folate- extremely stable with long shelf life
35
Q

sugar

A
  • High blood glucose is associated with low HDL
  • More damaging than fats for cholesteroal levels
  • Fructose can increase LDL cholesterol, elevates risk for vascular disease
  • Low SES- filling up with cheap processed foods- high in bad fats and glucose
  • High SES- afford better diet
36
Q

cholesterol

A
  • PUFA show decrease in LDL and saturated can increase LDL
  • HDL – good cholesterol
  • LDL- bad cholesterol  stick to artery walls and lead to plaque build up
  • Olive oil- fights plaques, improves immune system, better vascular health
37
Q

timing

A
  • Nutrition (folate b12) very important before dementia is diagnosed midlife but probably limited value after diagnoses
  • Supplemenst probably do not work- best is whole foods
  • Brushing teeth, eating healthy fats
  • Hydration important for memory, protein intake important to tackle muscle wasting
38
Q

exercise

A
  • Lowers blood pressure
  • Reduce bad cholesterol
  • Reduce abdominal fat
  • Can improve blood flow to brain + improve vascular function (hypoxia) as well as as immune system
  • Can act directly in decreasing toxicity beta amyloid (plaques) increasing neurotransmitter synthesis
  • Can increase neurogenesis in hippocampus improving connections between neurons
39
Q

psychosocial factors

A
  • Depression is common cause of disability
  • Coping skills – CBT

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