Week 10

Question 1

older adults

Answer 1

65+

Question 2

young-old

Answer 2

65-74

Question 3

old-old

Answer 3

75-84

Question 4

oldest-old

Answer 4

85+

Question 5

DSM-5 dementia types

Answer 5

mild cognitive disorder
major cognitive disorder
delirium (reversible)

Question 6

major neurocognitive disorder

Answer 6

evidence of significant cognitive decline from previous level: valid report and objective assessment
cognitive problems: interfere with daily activities; don’t interfere exclusively within context of delirium; not better explained by another disorder

Question 7

mild neurocognitive disorder

Answer 7

evidence of modest cognitive decline from previous level: valid report and objective assessment
cognitive problems: do not interfere with daily activities; don’t interfere exclusively within context of delirium; not better explained by another disorder

Question 8

MCI types

Answer 8

amnestic vs nonamnestic MCI

Question 9

MCI risk factors

Answer 9

older age
APOE allele
vascular risk factors (T2DM, smoking, hypertension, obesity)
CVD

Question 10

MCI protective factors

Answer 10

education
cognitively stimulating activities
physical exercise
dietary factors
sleep

Question 11

AD

Answer 11

brain tissue irreversibly dies
death in 12Y
progressive cognitive deterioration in memory, language, praxis, visuospatial abilities, executive skills
insidious onset: symptoms have gradual onset over months/years (usually 2-3Y before diagnosed)

Question 12

Plaques and tangles in AD

Answer 12

neurons gradually die when genes like ApoE4 and other factors promote formation of beta-amyloid plaques
amyloid initially forms as amyloid precursor protein (APP); enzymes break APP into short fragments; the fragments clump together forming plaques
once plaques form, tau, a protein that stabilises a neuron’s lengthy arms, may start to break down
when tau no longer stabilises the axons, the neuron shrivers and dies, leaving behind its tangled carcass
this synaptic deficits and loss of neurons prompts cognitive decline

Question 13

Brain changes in AD

Answer 13

cortical shrinkage
enlarged ventricles
hippocampus shrinkage

Question 14

Pharmacological AD treatment

Answer 14

cholinesterase inhibitors and range of antipsychotics, antidepressants, benzodiazepines and sedatives
prevention focused so far on preventing beta amyloid not supported, so shifting focus to tau

Question 15

Lancet commission on prevention

Answer 15

35% of dementia cases could be prevented if these 9 modifiable risk factors were addressed:
education
hearing loss
hypertension
obesity
depression
physical inactivity
social isolation and diabetes

Question 16

Sleep intradaily variability

Answer 16

fragmentation

Question 17

rest-activity cycles

Answer 17

stable, robust rest-activity cycles appear protective for dementia onset and progression

Question 18

increased wakefulness=

Answer 18

increased neuronal activity
increased beta amyloid

Question 19

decreased SWA=

Answer 19

decreased glymphatic clearance
increased beta amyloid and tau
increased synaptic damage

Question 20

1. increased sleep/circadian disruption=

Answer 20

increased oxidative stress
increased inflammation
decreased synaptic homeostasis

Question 21

2. increased sleep/circadian disruption=

Answer 21

decreased cognitive function
increased cognitive decline
increased dissatisfaction with life
increased institutionalisation

Question 22

vascular dementia/CI

Answer 22

cognitive disorders related to cerebrovascular diseases and bleeds

Question 23

VD diagnostic criteria

Answer 23

cognitive decline form previous level of functioning
impairment in memory + 2/more cognitive domains (attention, processing speed, language, executive skills)
impacts ability to perform usual activities
cerebrovascular disease present: conditions affecting blood vessels and blood supply to brain (stroke, aneurysm)
relationship between cognitive decline and cerebrovascular disease inferred by onset of dementia
clinical features: gait disturbance, history of unsteadiness and falls

Question 24

Subcortical VD

Answer 24

widespread lesions in subcortical areas
reduced executive skills (inhibition, planning, sequencing, goal-directed behaviour, abstraction, attention)
slowed processing speed
memory impairment is mild

Question 25

FTD

Answer 25

loss of neurons in frontal and temporal regions, spectrum disorder
type based on which part of brain atrophy takes place in
younger onset 45-65 YO
death within 5-10Y (average 8)

Question 26

3 main clinical syndromes of FTD

Answer 26

behavioural variance FTD 50% (rest are language deficit types)
semantic dementia
progressive non-fluent aphasia

Question 27

behavioural variant FTD

Answer 27

progressive decline in interpersonal and executive skills
lack of inhibition
strong personality changes
assessed during consultation; MRI shows typical frontal and anterior temporal lobe atrophy
obsessive and ritual-like
distracted
poor verbal fluency

Question 28

semantic dementia (FTD)

Answer 28

progressive breakdown of semantic ability and meaning of language
can still produce language
MRI shows selective, asymmetric anterior inferior temporal lobe
can see faces, can’t recognise

Question 29

progressive non-fluent aphasia (FTD)

Answer 29

breakdown in production of language
effortful non-fluent monotone
motor mouth and jaw control affected
atrophy on MRI varied in extent and severity

Question 30

Delirium DSM-5

Answer 30

disturbance in attention and awareness
develops over short period of time (hours to few days), fluctuates throughout the day
change in cognition (memory deficits, disorientation, language, etc.)
not better explained by another pre-existing, established or evolving neurocognitive disorder
there is evidence that the disturbance is a direct physiological consequence of another medical condition