Lecture 15: Aging and Dementia

T/F: memory declines drastically with age

false

T/F: intelligence declines drastically with age

false

T/F: learning becomes more difficult as we age

false

T/F: there is nothing you can do to counter the memory, intelligence, and language deficits that come with aging

false

which kind of memory is impaired with age

episodic

which kind of memory is spared with age

semantic

which kind of memory is spared with age

short-term

which kind of memory is spared with age

long-term (recognition)

which kind of memory is impaired with age

long-term (free recall)

which kind of iq is impaired with age

nonverbal iq

nonverbal iq

fluid; capacity to reason and adapt to new situations

verbal iq

crystallized; knowledge/skills acquired through experience

which kind of iq is spared with age

verbal iq

ways to reduce cognitive decline

diet, exercise, complex activities, living in a favorable environment

T/F: iq does not drastically decline with age

true

T/F: dementia is a generic term, not a diagnosis

true

all the boxes someone must check to qualify for dementia

1. significant (2 STDEVs) cognitive decline in one or more domains (motor, sensory/perceptual, language, memory, higher cognitive functioning, personality/emotion)

2. interferes with independence in activities of daily living (I/ADLs)

3. not due to delirium

4. not due to psychiatric disorder

some ADLs

eating, bathing, getting dressed, toileting, getting around inside

some IADLs

grocery shopping, money management, preparing meals, getting around outside

T/F: dementia is not a disease, but a syndrome caused by many different diseases

true

cortical dementias affect which part of the brain

grey matter (cell bodies)

subcortical dementias affect which part of the brain

white matter (myelinated axons), basal ganglia, etc

PD is a (type) dementia

subcortical

HD is a (type) dementia

subcortical

PSP stands for

progressive supranuclear palsy

PSP is a (type) dementia

subcortical

CJD stands for

Creutzfeldt-Jakob disease

CJS is a (type) dementia

subcortical

AD is a (type) dementia

cortical

vascular dementia is a (type) dementia

mixed

CVD is a (type) dementia

mixed

MID is a (type) dementia

mixed

CVD stands for

cardiovascular dementia

MID stands for

multi-infarct dementia

two types of vascular dementias

CVD, MID

DLB stands for

dementia w/ Lewy Bodies

DLB is a (type) dementia

mixed

AD usually begins with impairments in which domain

memory

how to definitively diagnose AD

brain biopsy

probable AD conditions

• dementia

• decline in 2 or more domains

• progressive

• consciousness is okay

• age 40-90

• no other disorder that can explain deficits

• impaired ADLs, family history, lab tests

possible AD conditions

• dementia in the absence of other explanatory factors

  • if there are other factors, the cognitive deficits are more consistent with AD (aphasia, amnesia, agnosia, apraxia, etc)

probable level of certainty

more

possible level of certainty

less

which chromosome is APOE gene on

19

gene associated with late-onset AD

APOE

alleles of APOE gene

e2, e3, e4

e2 allele of APOE gene

protective against AD

e3 allele on APOE gene

plays no role in AD

e4 allele on APOE gene

most strongly associated with developing AD

most common APOE allele

e2

best combo of APOE genes

APOE2, APOE

worst combo of APOE genes

APOE4, APOE4

where is brain atrophy in AD

everywhere

which neurotransmitter system decays in AD

Ach

amyloid-beta plaque formation: explain

• amyloid precursor protein (APP) is cut by enzymes, forming protein fragments of differing lengths

  • enzymes: Alpha-secretase, Beta-secretase, Gamma-secretase

• types of protein fragments:

  • alpha and gamma = harmless

  • beta and gamma = TOXIC

neurofibrillary tangles: explain

• abnormal tau protein damages microtubules and forms tangles inside the neuron

• this process is a byproduct of AB plaque buildup

glutamate dysregulation: explain

exitotoxicity (too much excitation) leads to cell death

inflammation of p3 (alpha + gamma (harmless) protein)

impairs AB clearance and tau misfolding

AD is a diagnosis of ___

exclusion

which memory types are impaired with AD

episodic

which type of amnesia with AD

anterograde

which memory types are impaired with AD

semantic

which memory types are impaired with AD

long-term (delayed recall)

which memory types are spared with AD

short term

which memory types are spared with AD

procedural memory (priming, conditioning, etc)

T/F: semantic associative networks are spared in AD

false

anomic aphasia

word finding and naming difficulties

language impairments in AD’s early stages

anomic aphasia

language impairments in AD’s middle stages

comprehension

language impairments in AD’s middle stages

repeating information

language impairments in AD’s late stages

fluency

visual-spatial functioning in AD

everyday disorientation

attention in AD

declines as the disease progresses

disorientation in AD

wandering, confusion

motor and sensory functions in AD

relatively preserved, but declines as disease progresses; apraxia can occur

only impaired sense in AD

olfactory

differential diagnosis between ___ and dementia is often difficult

depression

depression or dementia: patient answers “idk” instead of trying to answer questions

depression

depression or dementia: patient conceals their amnesia

dementia

depression or dementia: rapid onset

depression

issues with pharmacologic treatments for AD

target the symptom, not the cause (the dementia itself)