Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Brain in Health & Disease > L9 - Alzeimer's > Flashcards

L9 - Alzeimer's Flashcards

You may prefer our related Brainscape-certified flashcards:
The Brain flashcards
1
Q

What are the symptoms of Alzheimer’s?

A

Forgetfulness
Confusion
Less movement
Loss of bodily function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the neuroanatomy of an Alzheimer’s patient?

A

Layers of neurons get thinner, big gaps in cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What did PET scans of someone going through Alzheimer’s show?

A

Loss of energy metabolism around brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the cellular changes in Alzheimer’s?

A

Beta- Amyloid plaques

tau tangles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where does tau build up?

A

Cortex
Hippocampus
Visual cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what does tau normally do?

A

Helps stabilise microtubules and axon transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What can indirectly cause hyperphosphorylisation of tau?

A

Oxidative stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What direct events can cause the hyper-phos of tau

A

Upregulating of tau kinases
Downreg of phosphatases
Mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does the LOF of tau cause?

A

Detachment of MT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What can the GOF of tau cause?

A

NFTs made of hyperphosphorylated tau sequester normal tau.

NFTs become physical obstacles of vesicles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How does tau normally function?

A

Gets in the way of cargo but is required for MT integrity

Usually dephosphorylated to move out the way for motor proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What do tau-P mutations cause?

A

More readily phosphorylated and lead to neurodegeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What first suggests the amyloid hypothesis exists?

A

Down’s syndrome leads to AD by 40, linked to chr 21

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What other proteins could affect tau phosphorylation?

A

GSK3, CDK5 AND MARK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What happened when amyloid-Beta was synthesised and put into cultures?

A

Toxic to neuronal cultures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What other 2 genes were found to be associated with early onset AD>

A

Prenenilin 1 and 2

17
Q

What did mutations in prenelinin cause?

A

Increased production of amyloid beta

18
Q

What do the presenilins code for?

A

Two secretases beta (BACE) and gamma wich process beta-amyloid prescursor protein

19
Q

How is the proteolysis of APP involved?

A

After APP produced it either produces neurtrophic, neuroprotective peptide or produces AB peptide
Depending on which secretase chops it first it can be good or bad

20
Q

What happens when alpha-secretase (ADAM) cuts first and what happens when BACE doe?

A

ADAM - beneficial

BACE - not good and impairs function

21
Q

How does cell-cell spread of amyloid-B happen?>

A

Produced exracellularly and wraps up in little vesicles which are taken up by other cells - propensity for damage to spread around the brain like a prion

22
Q

What was shown in animal models for a therapy for amyloid hypo and what is the problem with it?

A

Inhibitor of B-secretase reduced about of Ab being produced

Work agains many other proteins

23
Q

What has been suggested as another therapy for amyloid hypo?

A

Proteolysis of amyloid-b

24
Q

Why are amploid plaques so bad?

A

Form clumps and hen attract other molecules and becomes resistant to degredation

25
Q

What eznymes could be invovled in therapeutic degradation of amyloid?

A

Neprylysin and insulin degrading enzyme

26
Q

What does neprilysin do?

A

Breaks down oligomers and breaks down into fragments

27
Q

What do amyloid-b plaques do?

A

Might bind to post synaptic receptors affecting transmission

28
Q

How do the amyloid and tau hypos mix?

A

Need interaction between Ab and tau to make MT transport work?
May form complexs

29
Q

What do plaques and tau tangles cause in neurons

A

Dendritic degradation

30
Q

What is a gene associated with lae onset AD?

A

aPOLIPOROTEIN e - many variants with differing levels of death

31
Q

Which variants of apolipoprotein E are the best and worst?

A

2 and 3 are good, 4 is bad

32
Q

What is proposed to be the fuction of apolipoprotein E?

A

Clearance of cholesterol and possibly amyloid B and take it to blood

33
Q

How could AD be linked to alzeimers>

A

May be to do with clearance of cholesterol

Mutations in insulin signalling increases risk of dementia

34
Q

What is Liraglutide?

A

Diabetic drug that preserves mouse memory

35
Q

How is oxidative stress suggested to be linked to AD?

A

Amyloid-B possibly protects cells for ROS?

(with diabetes) = problems with sugar and fat metabolism puts stress on mitochondria

36
Q

How vaccination go with trying to help AD?

A

370 patients got inflammation of the meninges - microglia and t cells attacked the Ab42 vaccination
7 years later had lower amyloid b
Clinical trials of shorter peptides (long end was attacked)

37
Q

What is the cholinergic drug hypo?

A

Using inhibitors of ACh-esterase so ACh sits in synapses longer
Can be good, some useless

Brain in Health & Disease (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions