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PSYC211 > Lecture 9- Memory and Disease > Flashcards

Lecture 9- Memory and Disease Flashcards

1
Q

What is the most common form of dementia?

A

Alzheimer’s disease

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2
Q

What is dementia?

A

Dementia is the term used when a person experiences a gradual loss
of brain function due to physical changes in the structure of their
brain.

Symptoms:

  • Loss of memory
  • impaired reasoning
  • reduced language skills
  • loss of daily living skills.
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3
Q

What are the mild symptoms of Alzheimer’s Disease?

A
  • Confusion and memory loss
  • Disorientation; getting lost in familiar surroundings
  • Problems with routine tasks
  • Changes in personality and judgment
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4
Q

What are the moderate symptoms of Alzheimer’s?

A
  • Difficulty with activities of daily living, such as feeding and bathing
  • Anxiety, suspiciousness, agitation
  • Sleep disturbances
  • Wandering, pacing
  • Difficulty recognizing family and friends
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5
Q

What are the severe symptoms of Alzheimer’s?

A
  • Loss of speech
  • Loss of appetite; weight loss
  • Loss of bladder and bowel control
  • Total dependence on caregiver
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6
Q

How long in years does it take in Alzheimer’s disease to get from diagnosis to severe symptoms?

A

6-7 years

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7
Q

What test is commonly used in the diagnosis of Alzheimer’s disease?

A
  • Phonemic and Semantic Verbal Fluency (SVF)
  • Patients are asked to generate as many words as they can either starting with a certain letter of the alphabet (phonemic fluency) or belonging to a certain semantic category e.g. animals (semantic fluency).
  • Measure the number of correct words spoken by the patient in one minute
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8
Q

In Pakhomov et al (2016) what longitudinal changes were found in SVF tests?

A
  • All cognitively were normal (CN) at start -Assessed at ~15 month intervals and retrospectively reassigned to group
  • AD group performance went down a lot, those with minor cognitive impairment had slight decline, control line was relatively flat
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9
Q

What is the primary risk factor for Alzheimer’s disease?

A
  • Age: The likelihood of developing the condition doubles every five years after you reach 65 years of age
  • Creates a upwards curve
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10
Q

In what population is Alzheimer’s prevalence meant to keep increasing?

A

65 plus. 15-39 and 40-64 age groups only increase slightly.

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11
Q

What is the current prevalence rate of Alzheimer’s at age 85?

A

20%

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12
Q

What are the brain changes observed in Alzheimer’s?

A
  • Shrinkage of tissue/ cortex, especially the hippocampus (consistent with memory issues), temporal lobe is also often shrunk
  • Enlargement of ventricles
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13
Q

What are the two main neuronal defects found in Alzheimer’s disease?

A
  • Amyloid plaques: clusters sitting outside neurons/ cells

- Neurofibrillary tangles: Inside neurons, causing degradation

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14
Q

What causes the loss of the cholinergic projection neurons in the basal forebrain?

A
  • This is a brain change associated with Alzheimer’s disease
  • These neurons sit in the basal forebrain and project out to other cortex areas communicating via the neurotransmitter acetylcholine. In Alzheimer’s the release of acetylcholine is reduced meaning these is not as much communication across synapses.
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15
Q

How is mild to moderate Alzheimer’s disease sometimes treated in relation to the neurotransmitter acetylcholine?

A

-Under normal conditions acetylcholine carries a message across the synapse, and then is broken down by a cholinesterase.
-Therefore, an effective treatment for Alzheimer’s can be to use
Cholinesterase inhibitors (AChE-Is) such as Donepezil (Aricept), Rivastigmine (Exelon) and Reminyl (Galantamine).
-These drugs block cholinesterase, giving the acetylcholine extra time to transmit messages.
-Effective in prolonging functioning the early stages of the disease but by no means is a complete solution.

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16
Q

What is beta amyloid? What change to beta amyloid occurs in Alzheimer’s disease?

A

-Amyloid Precursor Protein (APP) is a protein that appears to
have an important role in synaptic plasticity.
-Beta Amyloid (Aβ) is produced when APP (precursor protein) is cut into segments (cleaved) by secretases.
-In AD, Beta Amyloid is overproduced. It forms fibrillar plaques on the outside surface of cells. Plaques are distributed throughout the cortex.

17
Q

Where does APP span before it is cleaved into beta amyloid protein?

A

The cell membrane

18
Q

What enzymes cleaves APP into beta amyloid?

A
  • First Alpha Secretase cuts APP at the level of the cell membrane
  • Beta Secretase and Gamma Secretase then come along and cut allowing the toxic Beta-Amyloid fragment to be produced.
19
Q

Why do beta-amyloid fragments from clumps or plaques?

A

Because they are sticky

20
Q

Does amyloid plaque location map well to Alzheimer’s symptoms? Have

A

Amyloid Plaque location doesn’t map well onto symptoms: Occur across the cortex not just in areas associated with memory i.e. the temporal lobe also some people have lots of plaques but cognitively are fine

21
Q

Have Clinical trials of drugs that target Beta Amyloid been successful? What is now the focus?

A
  • No, have been disappointing so far.
  • The drugs may be successful at clearing plaques but this has no effect in eleviating Alzheimer’s symptoms.
  • Recent focus is on targeting Beta Amyloid Oligomers
22
Q

Is the oligomer evidence legitimate?

A
  • Possibility that some of the oligomer evidence is fraudulent
  • The bands in the research looked identical like they had just been copy and pasted when they should have represented two separate proteins.
  • Millions of dollars spent following up on this work but it is fake= real consequences for real people
23
Q

What changes in the protein TAU are associated with Alzheimer’s?

A
  • Microtubules stabilized by molecule called tau
  • In Alzheimer’s tau loses ability and microtubules start to break down forming tangles inside the cell
  • Neuron falls apart due to no structural support
24
Q

Do the locations of neurofibrillary tangles map well to the symptoms of Alzheimer’s?

A

Yes. As Alzheimer’s progresses NFTs appear initially in the
transentorhinal (perirhinal) cortex and then in neighbouring regions.
NFT progression parallels cognitive deficits. This progression is labelled in terms of Brak stages after the scientist who discovered the link.

25
Q

What test was used to see the Relationship between the extent of NFTs and cognitive impairment? What was found?

A
  • Mini-mental state exam (test of cognitive impairement).
  • Found that are the Brak stage increased (NFTs got worse) the score on the MMSE got worse going right down to zero at the severe end.
26
Q

What is the difference between early and late onset of Alzheimer’s?

A
  • Early onset= earlier than 65 years. Occurs in less than 5% of cases.
  • Late onset= over 65 years.
27
Q

Other than age what is also a risk factor for Alzheimer’s?

A

Family history/genetic disposition:
People with relatives who developed Alzheimer’s disease are
more likely to develop the disease themselves.

28
Q

Within Alzheimer’s cases influenced by family history/ genetics what are the two categories and frequencies? Additionally what gene mutations are invovled?

A

-Familial (early onset) AD (~3% of cases):
50% chance; early onset
Linked to mutation on PSEN1, PSEN2, APP genes

-Late onset(sporadic) AD (~97% of cases)
Risk is related to variations of the APOE gene on chromosome 19

29
Q

What variations are there of the APOE gene? What one is associated with sporadic AD?

A

-There are three major variations (alleles) of the APOE gene- called APOE2, APOE3 and APOE4. We are each born with two alleles at the APOE gene that we inherit from our parents.

-We can have any combination of the three variations:
For example, we could have E2/E2; E2/E3; E3/E3; and so on.

-E4 is the allele you don’t want!
Having one E4 confers 2-3 x higher risk
Having E4/E4 confers 5-8 x higher risk

-These APOE gene alleles produce slightly different forms of the Apolipoprotein E (ApoE) protein. ApoE is mainly produced by astrocytes, and transports cholesterol to neurons (providing neuronal support).

30
Q

What type of Alzheimer’s can we test for? Is it worth it?

A
  • Can test for the APOE4 gene to see if you have an increased risk of the sporadic form of Alzheimer’s
  • There is real debate about getting tested though as there is not a lot that can be done once the results are known. There is no treatment and it could just mean individuals live in fear. This however, may change once new research comes out- knowing early might become more useful.
31
Q

Is it just that those with the APOE4 gene are more likely to develop Alzheimer’s or are there other disadvantages? In what group is the risk more prominent?

A
  • They also are more likely to develop Alzheimer’s at an earlier age
  • This risk is more pronounced for females than males
32
Q

What are the effects of APOE4 on human brain cells in culture?

A

-Astrocytes:
Reduced APOE level
Cholesterol accumulation
Impaired amyloid beta clearance

-Neurons:
Increased synapse formation
Elevated early endosomes
Increased amyloid beta production

-Micro-glia like cells:
Immune prone
Reactive
Impaired amyloid beta clearance

33
Q

What is the link between APOE4 and the Blood-Brain Barrier (BBB)?

A
  • The BBB separates the circulation from the brain, allowing for protection from and transport regulation of serum factors and neurotoxins.
  • The BBB is not just a physical barrier but also acts more selectively as a transport interface, a secretory body, and a metabolic barrier (containing and releasing certain enzymes locally).

-The gene variant APOE4 is associated with a disruption of tight
junctions, which opens up the BBB

-APOE4 was associated with higher BBB permeability in hippocampus and parahippocampal gyrus – independent of amyloid and Tau accumulation

34
Q

What does elevated levels of a marker for pericyte injury predict? and among what group?

A
  • Elevated levels of a marker for pericyte injury predicts cognitive decline in APOE4 group
  • E.g. greater damage to pericytes= more leaky BBB= greater cognitive decline after 2 year period
35
Q

What study reveals a protection against AD? What about the participant group makes it such a useful study?

A
  • The University of Minnesota ‘Nun Study’ is a longitudinal study of aging and Alzheimer’s disease. Participants were 678 American members of the School Sisters of Notre Dame religious congregation who were aged 75 to 102 years of age .
  • Same diet, same exposure to environmental factors (valuable and rare in terms of controlling variables in study)
  • At 22 wrote an autobiography. Those who didn’t say much about themselves i.e had sparse/ low number or ideas had greater risk of AD when examined after death. In other words the brain weighed less and had more tangles in hippocampus + neocortex
  • This shows the physical brain status linked to how the individuals thought. Having complex ideas and creating lots of synapses helps to limit degeneration later on
36
Q

What are the Modifiable risk factors for dementia?

A 
poor education
midlife hearing loss (to do with less ability to interact socially?)
obesity and hypertension
late-life depression (to do with social interaction?)
smoking
physical inactivity
diabetes
social isolation
37
Q

What are higher idea density scores in early life associated with?

A

Intact cognition in late life despite the presence of AD lesions.

PSYC211 (23 decks)

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