Alzheimers disease Flashcards

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1
Q

what happens when the number of cholinergic neurons is decreased in the brain?

A

causes AD because there are no neurotransmitters (acetylcholine) sending signals through the synapse.

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2
Q

types of dementia

A

AVHAFCL
- AD (plaques and tangles)
- Vascular dementia (decrease circulation to brain)
- HIV/AID dementia (adv HIV and AIDS)
- Alcohol related dementia (deficient in vitamin B1)
- Front temporal lobar degeneration
- Creutzfeldt-jacob dementia (presence of prion particles)
- Lewy bodies dementia (protein aggregates affecting brain cells)

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3
Q

area of brain affect by AD

A

CBH
Cerebral cortex - thought, language and reasoning
Basal forebrain - personality, movement and judgement
Hippocampus - learning, memory

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4
Q

symptoms of moderate AD?

A

WDI
- worse memory loss
- depression and confusion
- increased relance on family members for decisions

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5
Q

symptoms of late AD?

A
  • loss of long term memory
  • unaware of time and place
  • doesn’t know family
  • unlearn basic motor skills (teeth brushing and hair brushing)
  • death 5-15 years of diagnosis
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6
Q

symptoms of early AD?

A

MHP
- memory loss of recent events
- hard learning new info
- personality change

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7
Q

How do you know if the diagnosis is correct?

A

after death when there is a brain tissue examination.

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8
Q

diagnosis of AD

A

there are no single test to find out if you have AD.

But they would:
- detailed medical history
- physical and neurological examination
- intellectual test
- psychiatric assessment
- neuropsychological test
- multiple types of scans PET, MRI and CT

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9
Q

what is the treatment of AD

A

There is no cure, they just manage the treatment:
- cholinergic (produces acetylcholine) drugs could be used for improving cognitive function in moderate or early AD.
- drugs for depression or deep deprivation
- community support

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10
Q

What is a acetylcholine?

A

it is a type of neurotransmitter, that helps with memory and muscle contraction.

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11
Q

what is amyloid plaque function?

A

extracellular, made up beta amyloid peptide (40 or 42aa), originates from the amyloid precursor protein (695 n 770aa) located on the chromosome 21. 42aa is a harmful peptide

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12
Q

what is the neurofibrillary tangles as hallacks of AD?

A

intracellular, cluster of protein inside the neuron, tau proteins (stabilize microtubules)

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13
Q

what are the effect of cholestral in AD?

A

having high cholesteral can increase the changes of having some type of dementia.

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14
Q

What are the effects of ApoE4 in AD?

A

ApoE4 is a genetic risk factor, that interacts with beta amyloid (toxic 42) and causes an increase in the development of plaques.

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15
Q

what are the financial effects of AD?

A

$1 in every $40 from the Australian health system is spent on AD.
The cost to the economy is at millions per year are spent on AD.

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16
Q

What percentage of change in AD in cause of death from 2000 to 2019?

A

increased by 145.2%

17
Q

what do caregivers support with for AD patients?

A

feeding, dealing with incontinence, bathing showering and getting to and from toilet .

18
Q

how does the abeta plaque process occur?

A

The APP with the beta secretase followed by the gema secretase cutting of the peptide cause a harmful beta amyloid peptide 42aa. Alot is developed and cause the sticking of the plaques together.

The alpha secretase is harmless.

19
Q

how does the neurofibrilliary tangle process occur?

A
  • when the tau protein increase causing the change of microtubules structure which causes the tau to accumulate which ruins the shape of the microtubules causing the tangles.
  • neurotoxcity induces cleavage of p35 to p25 to caplain.
20
Q

what genetic mutations contribute to AD?

A
  • being female
  • if you have down syndrom as you have 3 chromosomes of 21 which increases the chance of developing AD.
21
Q

what is dementia?

A

progressive decline in cognitive function.
due to damage in the brain tissue and it is faster than normal

22
Q

manifestation of dementia?

A

MMD
memory loss
mood swings
deficit in language

23
Q

cause of AD

A

neural loss together with amyloid plaque and neurofibrillary tangles.

24
Q
  1. types of AD
A

Familial (early)- one other family person with the disease.
Sporadic (late)- no one else with the diseases

25
Q

pharmocology of AD includes 2 factors and their role

A

AN
Acetylcholinesterase inhibitors - decrease destruction of acetylcholine.
NMDA antagonists - decrease overstimulation of glutamate
- their role is to increase acetylchloline levels

26
Q

why do people with down syndrome have AD sooner?

A

because they have x3 chrom 21 which increases gene for bAPP cause early onset AD.

27
Q

what the main component of the tangle?

A

hyperphosphoralted tau

28
Q

activation of the protein kinase cdk5 causes

A

tau phosphorylation and neural apoptosis.