Quiz 6 Flashcards
Brain Research Hypothesis
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)
STAC MODEL
Shares same features of BRH, same moderating relationship…where scaffolding (reserve) contributes to compensation reducing relationship between brain damage and cog. impairment
Reserve as a moderator
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
Testing BRH (three measures)
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)
Measuring Reserve
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
Measuring reserve in brain pathologies
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)
Factors contributing to increased cog. reserve
Genetics Socioeconomic status IQ Education Sleep Social Engagement Cognitive Stimulation Brain Games debate Healthy lifestyle Omit bad habits Diet Exercise
Factors contributing to increased cog. reserve: Genetics
Our DNA can influence the extent in which our brain can endure damage
Factors contributing to increased cog. reserve: Socioeconomic status
Health related, what you eat, doctors you see as a child, exercise…cog stimulation like music classes and being put into extraciriculars
Factors contributing to increased cog. reserve: IQ
some level of innate intelligence can contribute to CR
Factors contributing to increased cog. reserve: Education
KIND OF IN OUR CONTROL
what you can do with education moving forward
Factors contributing to increased cog. reserve: Sleep
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
Factors contributing to increased cog. reserve: Social Engagement
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
Factors contributing to increased cog. reserve: Cognitive Stimulation
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
Factors contributing to increased cog. reserve: Brain Games debate
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
Factors contributing to increased cog. reserve: Healthy lifestyle
MOST IMPORTANT FOR KEEPING BRAIN HEALTHY AND STAYING COG. FIT
Factors contributing to increased cog. reserve: Omit bad habits
No smoking/ drinking a lot
Factors contributing to increased cog. reserve: Diet
LOTS of water, fruits/vegetables, mediterranean diet???
Factors contributing to increased cog. reserve: Exercise
Any is good but AEROBIC IS BEST
Can help “regrow” brain
ALSO VERY IMPORTANT
“Selective” effect of exercise on anterior hippocampus (what makes it “selective”)
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
Exercise intervention v. habitual exercise
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
Senile dementia of the Alzheimer’s type
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
Alois Alzheimer
German psychiatrist and neuropathologist, examined Auguste D and 1st diagnosis of AD
Auguste D
First patient diagnosed with AD
Had: trouble sleeping, language disruptions, delusions, “lost myself”
AD pathology: Atrophy
Of the affected regions, including degeneration in the temporal and parietal lobes, parts of frontal cortex/cingulate gyrus
Gray and white matter shrunk
AD pathology: Tau tangles
deposits of the protein TAU that accumulates inside of nerve cells themselves
AD pathology: Amyloid plaques
deposits of the protein beta-amyloid that accumulates in the spaces between nerve cells
AD pathology: Regional progression
Some people stop at the preclinical or MCI and never progress further
Normal –> Preclinical –> MCI –> Dementia
Progression diagnosis criteria: Preclinical v. Mild Cognitive Impairment v. Dementia
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
AD Effects on: Memory
(Early AD) New memories are lost first, older are lost later
Newer memories are more hippo dependent
AD Effects on: Executive function/working memory
(Early AD) selected aspects of EFs, particularly those involving changing from one task to another (set-shifting) and self-monitoring
AD Effects on: Visuospatial function
(Moderate AD) Difficulty with navigation, spatial layout, and directions
Following the progression (visual spatial is in the back of the brain)
AD Effects on: Language
(Moderate AD) Naming and verbal fluency impairment
AD Effects on: Attention
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
Treatment options for AD
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
Why are hidden upsides hidden? (Reduced Inhibition)
reduced inhibition –> improved Memory for some background content –> inc performance if it ends up being relevant
Why are hidden upsides hidden? (Gist processing)
inc gist processing –> better ability to see the “big picture”
Why are hidden upsides hidden? (Life experience/wisdom)
More ‘life experience’ –> greater opportunity to amass wisdom
