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

Chapter 7/17/18 - Aging and Cognition Flashcards

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?

A
  1. Senile plaques - B Amyloid
  2. Neurofibrillary Tangles - Tau
  3. Basal forebrain degeneration
25
Q

What are the structural abnormalities observed with Alzheimer’s Disease? Hint: These areas regulate memory, attention, behaviour and emotions

A

1) Neocortex, entorhinal area, hippocampus, amygdala

2) Nucleus basalis, anterior thalamus, locus coeruleus, raphe nuclei

26
Q

Where are signs of AD first noticed in?

A

Entorhinal cortex, then proceed to hippocampus

27
Q

Changes can begin how many years before symptoms appear?

A

10-20

28
Q

What begins to shrink as more neutrons stop working and die?

A

Cerebral cortex

29
Q

What are mild AD signs?

A

Memory loss, confusion, trouble handling money, poor judgement, mood changes, anxiety

30
Q

What are moderate AD signs?

A

Increased memory loss, problems recognizing people, troubles with language and thoughts, restlessness, repetitive statements

31
Q

What occurs in the brain in severe AD cases?

A

Extreme shrinkage of brain

32
Q

What are severe AD symptoms?

A

Weight loss, seizures, skin infections, groaning, increased sleeping, loss of bladder control

33
Q

Death usually occurs due to what for those with severe AD?

A

Aspiration pneumonia

34
Q

Death usually occurs due to what for those with severe AD?

A

Aspiration pneumonia

35
Q

What results in cytoskeleton abnormalities?

A

Dysfunction and death of neutrons

Decrease in synaptic proteins in terminals

36
Q

Which cells are mostly affected in AD?

A

Large glutamatergic pyramidal cells in cortex and hippocampus
Cortical interneurons
Cholinergic neurons

37
Q

What are neurofibrillary tangles?

A

Fillamentous inclusions in cell bodies and proximal dendrites

38
Q

Where can neurofibrillary tangles also be found?

A

Axons and terminals (dystrophic neurites)

Dendrites (neuropil threads)

39
Q

Tangles are made by….

A

an isoform of tau clumping together

40
Q

What is tau?

A

A stabilizing component of microtubules

41
Q

How does AD tau differ from normal tau?

A

Normally soluble, but AD isoform is insoluble

Causes microtubules to collapse

42
Q

Tau first appears where?

A

Entorhinal cortex then later in neocortex

43
Q

What does neurofibrillary tangles disrupt?

A

Axonal transport

Neurons die but tangles are left behind

44
Q

What is the precursor protein to amyloid plaque?

A

Amyloid precursor proteins (APP)

45
Q

How are senile plaques formed?

A
  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
Q

Which part of the brain does senile plaques effect?

A

Hippocampus and other areas of cerebral cortex

47
Q

Which part of the brain does senile plaques effect?

A

Hippocampus and other areas of cerebral cortex

48
Q

What is the process for a mature senile plaque to be formed?

A
  1. ABeta appears (deposition of amyloid)
  2. Mature plaque, glial cells, swollen axons (senile plaque formation)
  3. Fibrillar Abeta surrounded, tangles (mature plaque)
49
Q

What genetic risk factors are involved in early onset of AD?

A
  1. Mutation of APP gene
  2. Mutation of presenilin 1 gene
  3. Mutation of presinilin 2 gene
50
Q

What other genetic risk factors are involved?

A

Certain alleles for ApoE

Mutation of alpha-2-macroglobulin

51
Q

A mutation in APP leads to…?

A

Increased ABeta production

52
Q

Presenilin 1 and 2 are inherited in what fashion?

A

Autosomal dominant

53
Q

Presenilin 1 and 2 promote the formation of what?

A

Toxic ABeta

54
Q

What is ApoE? What is its normal function?

A

Large protein that carries cholesterol in blood

Normally breaks down beta-amyloid

55
Q

What are the three different alleles known for ApoE? Which is the most common in normal populations? In AD populations?

A

ApoE3 (most common)

ApoE4 (rare but common in AD)

56
Q

How might an alpha-2-macroglobulin mutation affect ABeta deposits?

A

Affects removal

57
Q

Which two enzymes cleave amyloid precursor protein? What does this produce?

A

Beta-secretase and presenilin

Produces beta-amyloid

58
Q

What leads to the formation of plaques?

A

Beta-amyloid

59
Q

What is a response to plaques?

A

Neurofibrillary tangles

PSYC 375 (4 decks)

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