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Flashcards in alzheimer's disease Deck (40)
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1
Q

what kind of disorder is AD

A

terminal and progressive

degenerative

2
Q

state symptoms of AD

A

decline of memory
deficits of attention
personality changes q

3
Q

what are the final symptoms of AD

A

poor swallowing and loss of bladder control

4
Q

state immediate symptoms of AD

A

confusion and anxiety

5
Q

what is MMSE

A

mini mental state examination

6
Q

how is the MMSE used

A

patient asked to complete several tasks

score formed from performance

7
Q

what does the MMSE diagnose

A

possible cog impairment - PP would need further testing for diagnosis

8
Q

state changes in the neuropathology of a person with AD

A

hippocampus shrinks
enlarged ventricles
shrinkage of cerebral cortex

9
Q

define neuropathology

A

brain anatomy

10
Q

what are amyloid plaques

A

lumps of scar tissue made of degenerating neurons and the protein amyloid

11
Q

how does an alpha beta plaque form

A

amyloid precursor is broken down by enzymes

alpha and beta stick together to from plaque

12
Q

what is the genetic explanation of AD

A

result of mutations of amyloid precursor protein

13
Q

define transgenic

A

introduce genes of another species to another animal

14
Q

how can we study amyloid plaques

A

make transgenic mice

15
Q

describe the process of making transgenic mice

A

gene mutation that promotes build up of amyloid injected into animal

16
Q

what would occur in the offspring of transgenic mice (mice have gene mutation for growth of amyloid

A

offspring would also have gene mutation of amyloid

offspring produce similar brain to AD human patients

17
Q

what is the similarity with AD human patients and transgenic mice who have amyloid gene mutation

A

both produce similar brain activity of AD

18
Q

what is a high concentration of amyloid plaques associated with

A

neuron loss and memory disturbances

19
Q

which brain region can have a high concentration of amyloid plaques

A

medial temporal love

20
Q

what would happen if you inject animals with TAU gene

A

neurofibrillary tangles would be displayed

21
Q

what are neurofibrillary tangles

A

TAU protein

22
Q

what are microtubules

A

sticks - part of exoskeleton which forms shape

23
Q

what does the term MAP stand for

A

microtubule associated proteins

24
Q

how are neurofibrillary tangles formed

A

TAU becomes muddled and tangled up

microtubule degenerate and neuron die

25
Q

what happens if the microtubule degenerates

A

neurons die

axons structure is no longer supported

26
Q

what is apoE composed of

A

3 alleles of the same gene

E2, E3 E4

27
Q

what characterisics of E4?

A

bad gene

increased risk factors

28
Q

state characteristics of E2 gene

A

good gene

copies of this gene won’t increase risk factor

29
Q

what is E4 involved for?

A

involved in transport of cholesterol

increase risk factor of heart disease

30
Q

what things are prevalent in the medial temporal lobe

A

neuro tangles, amyloid plaques and neuron loss

31
Q

state 2 drugs that treat AD symptoms

A

cholinetserase inhibitor

NDMA receptor

32
Q

what effect does acetycholine have

A

reduce levels of AD in patients brain

33
Q

what is the cause of anterograde amnesia

A

acetycholine depletion

34
Q

what does the cholinergic system in AD patients result in

A

cell death and neuron loss

degeneration of basal ganglia

35
Q

what does cholinesterase inhibit

A

cholinesterase

36
Q

where is the main source of acetycholine

A

forebrain

37
Q

what is the function of cholinesterase

A

enzyme that breaks down acetate and choline

38
Q

what happens when glutamate becomes overexcited

A

cause an influx of calcium

39
Q

explain the process of neural stem cell transplants to improve AD cognitions

A
  1. stem cells injected
  2. stem cells become neuron and glial cells
  3. stem cell partially resolve memory functions
40
Q

what does the antagonist mematine (exiba) do?

A

block mematine and stop gluaminergic toxins