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PSYC 211 > L9 > Flashcards

L9 Flashcards

1
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.

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2
Q

what are some of the causes of dementia

A

the most common is
Alzheimer’s disease. Other causes include vascular dementia, dementia with Lewy bodies and fronto-temporal dementia.

All of them are slightly different but they cognitive symptoms are simmerler

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3
Q

what are some symptoms of dementia

A

loss of memory

impaired reasoning

reduced language skills

loss of daily living skills.

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4
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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5
Q

what are the moderate symptoms of alzheimer’s disease

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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6
Q

how long does it take to go from mild to moderate symptoms of alzheimer’s disease

A

this disease is progressive therefore over a period of 1 to 2 years

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7
Q

what are the severe symptoms of alzheimer’s disease

A

Loss of speech

Loss of appetite; weight loss

Loss of bladder and bowel control

Total dependence on caregiver

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8
Q

how long does it take from when you see the first sign of cognitive symptoms until death (the progression of the disease)

A

5 -6 years

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9
Q

what are phonemic and semantic verbal fluency (SVF) tests used for

A

Tests of phonemic and semantic verbal fluency (SVF) are widely used
in the assessment of individuals with memory complaints and in the
clinical diagnosis of Alzheimer’s disease.

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10
Q

what consists of phonemic and semantic verbal fluency (SVF) tests

A

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).

they measure the number of correct words spoken by the patient in one minute.

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11
Q

what is the longitudinal change in semantic verbal fluency in dementia patients

A

the results decline as time goes on.

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12
Q

what is the primary risk factor of alzhimers

A

age

The likelihood of developing the condition doubles every five years after you reach 65
years of age

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13
Q

describe the prevalence of Alzheimer’s disease

A

At 60 the proportion is very low (almost 0) and then it grows exponentially

The age that people are living to is longer therefore there are more people are getting this

On the right is the number of cases world wide and this is also growing exponentially

This increases is because of a change in demographics

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14
Q

in NZ what is the current prevalence of people at age 85 or above

A

20%

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15
Q

what are brain changes observed in AD

A

extreme shrinking of the hippocampus

enlarged ventricles

shrinking of tissue (the gaps between the folds are enlarged)

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16
Q

what do we think causes AD

A

plaques and neurofibrillary tangles

there is also a loss in cholinergic projection neurons of the basal forebrain

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17
Q

where are plaques and neurofibrillary tangles located

A

plaques are located outside the neurons in the extracellular space

tangles are inside the neurons

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18
Q

what is the effects of the loss in cholinergic projection neurons of the basal forebrain

A

the nuclei here have axons that projects out to wider areas and release ACh

ACh enhances memory as it facilitates transmission strengthening the synapse. therefore less ACH = less strong synapses

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19
Q

what is ACh broken down by

A

cholinesterase

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20
Q

what is used to treat mild to moderate AD

A

cholinesterase inhibitors

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21
Q

how do cholinesterase inhibitors work

A

They block cholinesterase, giving the acetylcholine extra time to transmit messages

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22
Q

what are some examples of cholinesterase inhibitors

A

Donepezil (Aricept),

Rivastigmine (Exelon)

Reminyl (Galantamine)

23
Q

are cholinesterase inhibitors an effective treatment for AD

A

no, they don’t have too much of a dramatic effect and they only show that small effect for the first 2 years of AD development

24
Q

what is Amyloid Precursor Protein (APP)

A

Amyloid Precursor Protein (APP) is a protein that appears to

have an important role in synaptic plasticity and it appears in many areas of the brain

25
Q

what is Beta Amyloid (Aβ)

A 
Beta Amyloid (Aβ) is produced when APP is cut into segments
(cleaved) by secretases.
26
Q

what is APPs and Aβs effect on AD

A

In AD, Beta Amyloid is overproduced. It clumps together and forms fibrillar plaques on the outside surface of cells. these plaques are distributed throughout the cortex and are toxic (they start to kill neurons)

27
Q

why is Beta Amyloid not over produced in a healthy brain

A

because AAP is usually cleaved by alpha scrotase at the part of the protein which would become the middle of Aβ

getting cleaved in the middle of Aβ means that it wouldn’t never be able to form

28
Q

what causes the over production of Aβ in AD

A

beta and gamma secretase cleave AAP in a way that Aβ is formed

29
Q

what does the distribution of Aβ across the brain tell us

A

Amyloid Plaque location doesn’t map well onto symptoms

therefore when you look at the distribution of Aβ and where they are damaging in the brain it doesn’t add up to what the symptoms of AD are

30
Q

what is Aducanumab (2021)

A

New drug that has just received FDA approval for treatment of AD

What it is effective in is removing the plaques from the brain but removing these doesn’t appear to have any effect on the cognition of the individuals

31
Q

what is the role of tau proteins in a healthy brain

A

they hold the microtubules together it their tubal structure

32
Q

what is Taus effect in AD

A

Microtubules are the scaffold of the neurons.

What happens in AD is the the Tau protein gets phosphorylated and the tou forms clumps inside the cell called neurofibrillary tangles (NFTs)

You then have a disruption in the microtubules as they fall apart and no longer make connections with other neurons

This degeneration does map well with the symptoms

33
Q

what are the clumps of Tau protein called

A

neurofibrillary tangles (NFTs)

34
Q

where do neurofibrillary tangles (NFTs) initially appear in AD progression

and then as it progresses

A

As Alzheimer’s progresses NFTs appear initially in the
transentorhinal (perirhinal) cortex. this is where information from the cortex goes into the hippocampus

As the disease progresses then the tangles start to go into the hippocampus and then in neighbouring regions.

NFT progression parallels cognitive deficits

35
Q

is the relationship between NFTs and the symptoms of AD seemingly casual

why

A

the more NFTs you have the worse cognitive impairments you have on a Mini mental state exam

36
Q

what are the major risk factors

A

age (5% < 65 years)

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

Familial (early onset)
- only makes up 2-3% of cases BUT if someone in your family has it it increases your likelihood by 50% chance for early onset

37
Q

what are the genetic factors of AD linked to

A

linked to mutation on PSEN1, PSEN2, APP genes

38
Q

when is AD classified as early onset

A

when you see symptoms before 65

39
Q

what is late onset (sporadic) AD risk factors related to

A

risk is related to variations of the APOE gene on chromosome 19

40
Q

how do variations of the APOE gene on chromosome 19 increase your chances of developing late onset (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.

Having one E4 confers 2-3 x higher risk

Having E4/E4 confers 5-8 x higher risk

41
Q

what does the APOE gene cause

A

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

42
Q

APOE possibly has more effect on females than males

A

i’m not sure theres a graph in the lecture but IDK what it wants from me

43
Q

what is the problem with APOE in astrocytes

A

reduction in APOE level causing cholesterol accumulation and impaired beta amylase clearance

44
Q

what is the problem with APOE in microglia like cells

A

they become immune prone (over reactive) and have impaired beta amylase clearance

45
Q

what is the problem with APOE in neurons

A

increased synapps formation

elevated rely endosomes

increases formation of beta amylase

46
Q

what is the blood brain barrier

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)
47
Q

what is APOE4s effect on the BBB

A

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

48
Q

capillaries are usually just the basement membrane and the endothelial cells which have an intracellular space separating them

what is different about capillaries in the brain

A

then endothelial cells are held together via tight junctions

the capillaries is also covered by astrocytes for support and then pericytes for maintaining that support

49
Q

how does APOE4 cause AD

A

the BBB is leaky which leads to elevated levels of a marker for pericyte injury predicts cognitive decline

50
Q

what is the progression of AD

A

you see the first cognitive symptoms after 1-2 years (therefore it is developing for about 1-2 years before you get a diagnosis)

51
Q

what was the nun 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 .

52
Q

why is the nun study so good

A

because early life autobiographies were obtained at average age 22

They had been in this order for a long period of time. They have had the same diet and the same environmental exposure because they have lived in the nunnery since that were 20

53
Q

what did the nun study find

A

The more ideas they had when they were 20 years old the less likely they were to develop AD

therefore this suggests that the things you did in your 20s has an effect on if you were developing AD

Therefore we believe that having a good education protects you from AD (more ideas)

54
Q

what is the cognitive reserve hypothesis

A

that education is a protective factor against AD

PSYC 211 (26 decks)

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