Quiz 6 Flashcards

1
Q

Brain Research Hypothesis

A

Focused on the relationship between brain damage –> outcome
Says that neural structure is related to cognition HOWEVER there is a dissociation between brain damage and cog. outcomes (relationship is not as strong)

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2
Q

STAC MODEL

A

Shares same features of BRH, same moderating relationship…where scaffolding (reserve) contributes to compensation reducing relationship between brain damage and cog. impairment

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3
Q

Reserve as a moderator

A

BRH says that brain reserve may function as a moderator, meaning that an inc. in reserve will influence the neural integrity and cog. function by reducing the relationship
Measures show that reserve is responsible for regulating the relationship between neural burden and decline

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4
Q

Testing BRH (three measures)

A

Reserve: eg. premorbid intelligence or education
Brain damage: brain atrophy or structure impairments
Change in cognitive capacity (aka outcome): need some type of metric to see if memory has changed over time (longitudinal measure)

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5
Q

Measuring Reserve

A

Structurally: ‘extra’ neurons and synapses, volume, head circumference, dendritic branching
Functionally: a degree of excess capacity or compensatory mechanisms such that the brain could continue to perform well despite damage

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6
Q

Measuring reserve in brain pathologies

A

See much greater damage in higher education because they were able to handle it longer without getting diagnosis
Memory seems great until a point than decreases fast (really good reserve)

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7
Q

Factors contributing to increased cog. reserve

A
Genetics
Socioeconomic status
IQ
Education
Sleep
Social Engagement 
Cognitive Stimulation 
Brain Games debate
Healthy lifestyle
Omit bad habits
Diet
Exercise
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8
Q

Factors contributing to increased cog. reserve: Genetics

A

Our DNA can influence the extent in which our brain can endure damage

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9
Q

Factors contributing to increased cog. reserve: Socioeconomic status

A

Health related, what you eat, doctors you see as a child, exercise…cog stimulation like music classes and being put into extraciriculars

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10
Q

Factors contributing to increased cog. reserve: IQ

A

some level of innate intelligence can contribute to CR

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11
Q

Factors contributing to increased cog. reserve: Education

A

KIND OF IN OUR CONTROL

what you can do with education moving forward

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12
Q

Factors contributing to increased cog. reserve: Sleep

A

getting sleep is critical to cognition
Provides brain a state optimal for consolidation and gist processing
supports creativity, Memory, and emotional regulation
“sleeping on it” can help solve problems

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13
Q

Factors contributing to increased cog. reserve: Social Engagement

A

interacting with people is important for well-being and cognition, related to inc. in cognition and brain volume, social support can buffer against the effects of stress

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14
Q

Factors contributing to increased cog. reserve: Cognitive Stimulation

A

on its own is very important, this is what is the use it or lose it talks about, need to keep using our brain or it will atrophy

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15
Q

Factors contributing to increased cog. reserve: Brain Games debate

A

Brain training has benefits to cognition…BUT may not generalize to other activities in daily lives
Limited cognitive transfer so they are not necessarily better than “real world” cog activities
UPSHOT: they do stimulate brain

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16
Q

Factors contributing to increased cog. reserve: Healthy lifestyle

A

MOST IMPORTANT FOR KEEPING BRAIN HEALTHY AND STAYING COG. FIT

17
Q

Factors contributing to increased cog. reserve: Omit bad habits

A

No smoking/ drinking a lot

18
Q

Factors contributing to increased cog. reserve: Diet

A

LOTS of water, fruits/vegetables, mediterranean diet???

19
Q

Factors contributing to increased cog. reserve: Exercise

A

Any is good but AEROBIC IS BEST
Can help “regrow” brain
ALSO VERY IMPORTANT

20
Q

“Selective” effect of exercise on anterior hippocampus (what makes it “selective”)

A

Exercise ONLY influenced the anterior hippocampus
Anterior shows more atrophy and age related decay … important because usually this shows A LOT of loss for OAs but exercise can seem to protect it

21
Q

Exercise intervention v. habitual exercise

A

The exercise intervention lead to improvements, but in comparison to control (stretching) group it wasn’t a huge difference
A LOT of it had to do with the pre-experimental data

22
Q

Senile dementia of the Alzheimer’s type

A

SDAT; most common form of D
Incurable, degenerative, and terminal
Progressive: early stage- depression/small dec., intermediate- irritable, anxiety, deterioration of speech
advanced- simple responses are difficult

23
Q

Alois Alzheimer

A

German psychiatrist and neuropathologist, examined Auguste D and 1st diagnosis of AD

24
Q

Auguste D

A

First patient diagnosed with AD

Had: trouble sleeping, language disruptions, delusions, “lost myself”

25
Q

AD pathology: Atrophy

A

Of the affected regions, including degeneration in the temporal and parietal lobes, parts of frontal cortex/cingulate gyrus
Gray and white matter shrunk

26
Q

AD pathology: Tau tangles

A

deposits of the protein TAU that accumulates inside of nerve cells themselves

27
Q

AD pathology: Amyloid plaques

A

deposits of the protein beta-amyloid that accumulates in the spaces between nerve cells

28
Q

AD pathology: Regional progression

A

Some people stop at the preclinical or MCI and never progress further
Normal –> Preclinical –> MCI –> Dementia

29
Q

Progression diagnosis criteria: Preclinical v. Mild Cognitive Impairment v. Dementia

A

Preclinical: silent phase- brain changes without noticeable symptoms, not detectable on tests
MCI (Mild cognitive impairments): cog changes are of concern to individual or fam, 1+ cog domains significantly impaired, quantifiable on tests
Dementia: drops off quickly and progressive, cog impairment severe enough to interfere with daily activities

30
Q

AD Effects on: Memory

A

(Early AD) New memories are lost first, older are lost later

Newer memories are more hippo dependent

31
Q

AD Effects on: Executive function/working memory

A

(Early AD) selected aspects of EFs, particularly those involving changing from one task to another (set-shifting) and self-monitoring

32
Q

AD Effects on: Visuospatial function

A

(Moderate AD) Difficulty with navigation, spatial layout, and directions
Following the progression (visual spatial is in the back of the brain)

33
Q

AD Effects on: Language

A

(Moderate AD) Naming and verbal fluency impairment

34
Q

AD Effects on: Attention

A

largely unaffected (unless task has to do with working memory). impairments in attention in an otherwise mildly impaired patient are used as a marker that the patient has a disorder other than AD

35
Q

Treatment options for AD

A

NO CURE for it or to stop progression
Some treatment includes medications and non-drug approaches to manage symptoms (anxiety/depression meds)
Advances in reducing amyloid build up
Trying to figure out biomarkers

36
Q

Why are hidden upsides hidden? (Reduced Inhibition)

A

reduced inhibition –> improved Memory for some background content –> inc performance if it ends up being relevant

37
Q

Why are hidden upsides hidden? (Gist processing)

A

inc gist processing –> better ability to see the “big picture”

38
Q

Why are hidden upsides hidden? (Life experience/wisdom)

A

More ‘life experience’ –> greater opportunity to amass wisdom