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PSYC 375 > Chapter 7/17/18 - Aging and Cognition > Flashcards

Chapter 7/17/18 - Aging and Cognition Flashcards

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1
Q

What did Baltimore’s study involve?

A

Longitudinal study of aging

2000+ people followed > 40 years

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2
Q

What did Baltimore’s study observe declines in?

A

Memory, visuospatial, verbal fluency, general IQ, in mid 60s

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3
Q

During the 3rd decade of life, what is observed?

A

Cells loss, synaptic loss (regional patterns!)

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4
Q

Which part of the brain is correlated with performance?

A

Hippocampal size

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5
Q

Which part of the brain is correlated with performance?

A

Hippocampal size

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6
Q

Some studies have found decreased brain activation during what?

A

Encoding and retrieval of information requiring self-initiated effort

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7
Q

When faces had to be learned, what was observed?

A

Less active frontal and temporal areas

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8
Q

Some studies reported higher activation levels though. What may this be the result of?

A

Effort

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9
Q

What are four other additional changes of CNS during aging?

A
  1. Motor skills - gait and stride
  2. Postural reflexes
  3. Sleep
  4. Brain weight decreases
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10
Q

What is loss with respect to sleep when aging?

A

Loss of stage 3,4, and REM sleep

More nocturnal waking

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11
Q

Brain weight decreases involves the loss of what?

A
  1. Neurons and neural connections

2. Enzymes that synthesize neurotransmitters (e.g. ChAT)

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12
Q

What are three ways to slow the effects of aging?

A
  1. Favourable environment
  2. Intellectually stimulating activities
  3. Having a partner with high I.Q.
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13
Q

What is a herb that is thought to decrease the occurrence of Alzheimer’s/dementia?

A

Ginkgo Biloba

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14
Q

What characterizes senile dementias?

A

Cognitive impairments and loss of memory that interfere with social/occupational function

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15
Q

What are some types and causes of senile dementias?

A 
Cerebrovascular disease
Lewy body dementia
Parkinson's
Alcoholism
AIDS
Syphilis
Brain tumor, vitamin deficiency
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16
Q

What is the most common senile dementia?

A

Alzheimer’s Disease (40% of people over 80)

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17
Q

What are the initial symptoms of Alzheimer’s Disease? Later symptoms?

A

Initial: Loss of memory for recent events
Later: Complete cognitive decline (progressive)

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18
Q

What is observed through a PET scan for those with Alzheimer’s?

A

Overall decrease in brain activity (temporal and posterior parietal lobes)
Cell loss in frontal, temporal, and parietal lobe

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19
Q

What is observed through a PET scan for those with Alzheimer’s?

A

Overall decrease in brain activity (temporal and posterior parietal lobes)
Cell loss in frontal, temporal, and parietal lobe

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20
Q

Treatments for senile dementias depend on what?

A

Cause

Case history, physical, psychological work up

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21
Q

What can occasionally be seen through using CT and MRI?

A

Mediotemporal lobe abnormalities

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22
Q

What can be seen through using PET, SPECT, fMRI?

A

Decreased blood flow to parietal and temporal lobes

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23
Q

When can senile dementia be definitively diagnosed?

A

Autopsies

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24
Q

What are the three main characteristics of Alzheimer’s Disease?

Study These Flashcards
A
  1. Senile plaques - B Amyloid
  2. Neurofibrillary Tangles - Tau
  3. Basal forebrain degeneration
25
What are the structural abnormalities observed with Alzheimer's Disease? Hint: These areas regulate memory, attention, behaviour and emotions
1) Neocortex, entorhinal area, hippocampus, amygdala | 2) Nucleus basalis, anterior thalamus, locus coeruleus, raphe nuclei
26
Where are signs of AD first noticed in?
Entorhinal cortex, then proceed to hippocampus
27
Changes can begin how many years before symptoms appear?
10-20
28
What begins to shrink as more neutrons stop working and die?
Cerebral cortex
29
What are mild AD signs?
Memory loss, confusion, trouble handling money, poor judgement, mood changes, anxiety
30
What are moderate AD signs?
Increased memory loss, problems recognizing people, troubles with language and thoughts, restlessness, repetitive statements
31
What occurs in the brain in severe AD cases?
Extreme shrinkage of brain
32
What are severe AD symptoms?
Weight loss, seizures, skin infections, groaning, increased sleeping, loss of bladder control
33
Death usually occurs due to what for those with severe AD?
Aspiration pneumonia
34
Death usually occurs due to what for those with severe AD?
Aspiration pneumonia
35
What results in cytoskeleton abnormalities?
Dysfunction and death of neutrons | Decrease in synaptic proteins in terminals
36
Which cells are mostly affected in AD?
Large glutamatergic pyramidal cells in cortex and hippocampus Cortical interneurons Cholinergic neurons
37
What are neurofibrillary tangles?
Fillamentous inclusions in cell bodies and proximal dendrites
38
Where can neurofibrillary tangles also be found?
Axons and terminals (dystrophic neurites) | Dendrites (neuropil threads)
39
Tangles are made by....
an isoform of tau clumping together
40
What is tau?
A stabilizing component of microtubules
41
How does AD tau differ from normal tau?
Normally soluble, but AD isoform is insoluble | Causes microtubules to collapse
42
Tau first appears where?
Entorhinal cortex then later in neocortex
43
What does neurofibrillary tangles disrupt?
Axonal transport | Neurons die but tangles are left behind
44
What is the precursor protein to amyloid plaque?
Amyloid precursor proteins (APP)
45
How are senile plaques formed?
1. APP sticks through neuron membrane 2. Enzymes cut APP into fragments (include beta-amyloid) 3. Beta-amyloid fragments come together in clumps (forms plaques) 4. Dystrophic axons surround deposits
46
Which part of the brain does senile plaques effect?
Hippocampus and other areas of cerebral cortex
47
Which part of the brain does senile plaques effect?
Hippocampus and other areas of cerebral cortex
48
What is the process for a mature senile plaque to be formed?
1. ABeta appears (deposition of amyloid) 2. Mature plaque, glial cells, swollen axons (senile plaque formation) 3. Fibrillar Abeta surrounded, tangles (mature plaque)
49
What genetic risk factors are involved in early onset of AD?
1. Mutation of APP gene 2. Mutation of presenilin 1 gene 3. Mutation of presinilin 2 gene
50
What other genetic risk factors are involved?
Certain alleles for ApoE | Mutation of alpha-2-macroglobulin
51
A mutation in APP leads to...?
Increased ABeta production
52
Presenilin 1 and 2 are inherited in what fashion?
Autosomal dominant
53
Presenilin 1 and 2 promote the formation of what?
Toxic ABeta
54
What is ApoE? What is its normal function?
Large protein that carries cholesterol in blood | Normally breaks down beta-amyloid
55
What are the three different alleles known for ApoE? Which is the most common in normal populations? In AD populations?
ApoE3 (most common) | ApoE4 (rare but common in AD)
56
How might an alpha-2-macroglobulin mutation affect ABeta deposits?
Affects removal
57
Which two enzymes cleave amyloid precursor protein? What does this produce?
Beta-secretase and presenilin | Produces beta-amyloid
58
What leads to the formation of plaques?
Beta-amyloid
59
What is a response to plaques?
Neurofibrillary tangles

PSYC 375 (4 decks)

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