Aging, MCI, dementia

Question 1

What happens with normal brain aging?

Answer 1

brain volume shrinks; dopamine and serotonin levels decline; cerebral blood flow decreases; accumulation of ischemic white matter lesions; mild AD pathology

Question 2

Which brain functions decline with age?

Answer 2

working memory, STM, LTM, speed of processing, but not verbal knowledge or wisdom

Question 3

Mild cognitive impairment

Answer 3

mild cognitive difficulties in excess of normal aging with preserved activities of daily living

Question 4

Prevalence of MCI

Answer 4

12-18% of people over age 60 globally

Question 5

Conversion rate of MCI to dementia

Answer 5

5-6% per year

Question 6

5 predictors of conversion of MCI to dementia

Answer 6

older age, high medical burden, APOE ε4 status (more copies of allele = higher risk), low education, low participation in leisure activities

Question 7

2 main types of MCI

Answer 7

amnestic (memory mainly affected) and non-amnestic (other cognitive functions affected)

Question 8

2 subtypes of amnestic and non-amnestic MCI

Answer 8

single domain and multi-domain

Question 9

Single domain amnestic MCI

Answer 9

only memory is affected; risk of AD

Question 10

Multi-domain amnestic MCI

Answer 10

memory and other domains are affected; risk of AD/VaD or vascular dementia

Question 11

Disease risks of single and multi-domain non-amnestic MCI

Answer 11

other dementias (e.g. FTD, DLB, PDD)

Question 12

Dementia

Answer 12

impairment of multiple cognitive functions and activities of daily living; an insidious decline from normal functioning

Question 13

Onset and course of dementia

Answer 13

onset in middle to late adulthood with a progressive course

Question 14

Which gender has higher risk of dementia?

Answer 14

females, because they live longer

Question 15

When does dementia prevalence begin to exponentially increase?

Answer 15

ages 70-79

Question 16

Modifiable risk factors of dementia in early and middle ages

Answer 16

less education and health problems (e.g. hearing loss, hypertension)

Question 17

Modifiable risk factors of dementia in later life (above 65)

Answer 17

health problems (e.g. smoking, depression, physical inactivity)

Question 18

5 ways to diagnose dementia

Answer 18

history of progression; neuropsychological confirmation; interview with collateral regarding ADL; MRI (regional atrophy); blood biomarkers and neuroimaging techniques specific for each type

Question 19

Prevalence of AD

Answer 19

7% of people over age 65

Question 20

Incidence of AD

Answer 20

14 per 1000 people over age 65

Question 21

Who is AD more common in?

Answer 21

females and APOE ε4 allele carriers

Question 22

Clinical presentation of AD in early stages

Answer 22

mild episodic memory deficit

Question 23

Clinical presentation of AD in middle stages

Answer 23

moderate-severe episodic memory deficit; semantic memory loss; non-fluent speech and/or visuospatial difficulties; executive dysfunction

Question 24

Clinical presentation of AD in late stages

Answer 24

symptoms in early and middle stages, apraxia, apathy, paranoia

Question 25

Macro or structural changes in brain with AD

Answer 25

progressive loss of connections between neurons and neurons themselves; brain shrinks; cerebral cortex shrivels and fluid-filled ventricles expand

Question 26

2 microscopic changes in brain with AD

Answer 26

peptide amyloid-β or plaques accumulate between neurons and microtubule-associated protein tau aggregate into neurofibrillary tangles inside neurons, which persist afters neurons die

Question 27

Prognosis of AD

Answer 27

typically starts in the medial temporal lobe 20 years before symptoms show the MCI converts into dementia within 4-8 years

Question 28

4 ways to diagnose AD and their biomarkers

Answer 28

MRI (medial temporal atrophy); PET (tau ligand binding in medial temporal lobes); Cerebrospinal fluid (elevated phosphorylated tau); Blood (low Aβ42/40 ratios)

Question 29

3 treatments for AD

Answer 29

acetylcholinesterase inhibitors (e.g. donzepil); glutaminergic antagonists (e.g. memantine); anti-amyloid antibody (e.g. aducanumab, lecanemab)

Question 30

How effective is lecanemab?

Answer 30

very effective in clearing amyloid plaques compared to a placebo

Question 31

Frontotemporal dementia

Answer 31

atrophy in the frontal and anterior temporal lobes in the brain

Question 32

3 main variants of FTD

Answer 32

language, behavioral, motor

Question 33

Clinical presentation of behavioral variant of FTD (bvFTD)

Answer 33

inhibition, apathy, social inappropriateness, executive dysfunction, anosognosia, preserved memory

Question 34

2 primary progressive aphasia variants in FTD

Answer 34

non-fluent aphasia (halting speech with agrammatism) and semantic dementia

Question 35

Semantic dementia

Answer 35

impaired confrontation naming, single-word comprehension, and object knowledge

Question 36

2 ways to diagnose bvFTD

Answer 36

neuropsychological testing and social cognitive testing

Question 37

Treatments for FTD

Answer 37

only symptom management due to diverse neuropathology each with different pharmacological agents needed

Question 38

Clinical presentation of lewy body dementia

Answer 38

fluctuations in attention and awareness; visuospatial difficulties; hallucinations; parkinsonism (symmetric); REM sleep behavior disorder

Question 39

Neuropathology of lewy body dementia

Answer 39

intracellular aggregation of α-synuclein especially in cortex, substantia nigra, limbic system, brain stem

Question 40

Treatments for LBD

Answer 40

acetylcholinesterase inhibitors; L-dopa for parkinson’s symptoms; NOT antipsychotics

Question 41

Clinical presentation vascular dementia

Answer 41

cumulative ischemic vascular disease and clinically symptomatic strokes; subcortical dementia profile; vascular risk factors; progressive or stepwise decline

Question 42

Clinical presentation of subcortical dementia

Answer 42

cognitive slowing, executive dysfunction, language, preserved visuospatial processing